Information

Spredning af en godartet virus i en befolkning over tid

Spredning af en godartet virus i en befolkning over tid



We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Dette er et lidt svært (for mig) befolkningsdynamikspørgsmål, og jeg spekulerer på, om nogen med erfaring på dette område kunne foreslå en fornuftig tilgang?

Mine simplificerende antagelser: Lad p(k) som en grov oversimplifikation være verdens befolkning ved generation k, og antag en jævn eksponentiel kurve, der modellerer p(k) fra $k=0$ ved 10.0000 f.Kr. til generation $k= 600$ i 2000 CE En generation er 20 år, og iht. med denne Wiki er der omkring 4 millioner individer ved $k=0$ og 6070 millioner ved $k=600.$ (Selvfølgelig er den eksponentielle model dårlig, da verdens befolkningstilvækst ser ud til at have været træg før den registrerede historie.)

Antag nu, at en godartet virus inficerer 120 individer i $k=0.$ Den inficerer godartet alle individer, der har mindst én inficeret forælder. Måske ligegyldigt, fortsætter den også med at inficere 30 nye individer per million i hver generation (fordi den findes i jorden), men ville ikke inficere dem, der allerede er udsat.

Kald inficerede individer II og ikke-inficerede NI. De kan ikke skelnes uden kliniske tests - som ikke udføres, da virussen er harmløs. Da II-individer er næsten sikre på at parre sig med NI-individer, vil antallet af II i tidligere generationer vokse meget hurtigt. I et stykke tid vil væksthastigheden af ​​II overstige den for p(k). På et tidspunkt vil det være usandsynligt, at et II-individ vil støde på en NI-kammerat, men nogle få NI-personer vil stadig danne par med NI-kammerater - i et stykke tid.

Mit spørgsmål er, efter 600 generationer, hvad er et rimeligt skøn over procentdelen af ​​II i befolkningen? Er det muligt, at der ville være nogen NI-individer tilbage? Eller ville vi have en form for dynamisk ligevægt mellem II og NI, hvor (tror jeg) førstnævnte ville dominere stærkt?

FWIW er befolkningsvækstmodellen $p(k)=4e^{0,012 k}$ med $p(k)$ i millioner.


For nemheds skyld betegner jeg populationen af ​​ikke-inficerede individer med $N$ og de inficerede med $I$.

Model uden jordinfektion

Da din fænomenologi er generationsbaseret, ville den bedste tilgang være at lave en iterativ populationsbaseret model. Lad os først glemme de nye infektioner med jord. Jeg vil først give dig ligningerne og derefter forklare dem: $$ egin{alignedat}{3} N_{k+1} &= & &g frac{N_k}{N_k+I_k}N_k & =~& g frac {N_k^2 {N_k+I_k}, I_{k+1} &= g I_k &~+~&g frac{I_k}{N_k+I_k}N_k &~=~& g frac{2N_kI_k+ I_k^2}{N_k+I_k}. end{alignedat} $$

  • $g=left(frac{6070}{4} ight)^frac{1}{600} ≈ 1,012$ er vækstraten pr. generation.

  • $frac{N_k}{N_k+I_k}$ er sandsynligheden for, at et givet ikke-inficeret individ parrer sig med et andet uinficeret individ. Nu har vi $N_k$ sådanne individer, og de ganges med $g$, og den næste generation af ikke-inficerede er således $g frac{N_k}{N_k+I_k}N_k$.

  • Inficerede-inficerede parringer producerer inficeret afkom regelmæssigt, hvilket tegner sig for $gI_k$-termen.

  • $frac{I_k}{N_k+I_k}$ er sandsynligheden for, at et givet ikke-inficeret individ parrer sig med et inficeret individ. Nu har vi $N_k$ sådanne individer, og de multipliceres med $g$ og dermed får den næste generation af inficerede en ekstra $g frac{I_k}{N_k+I_k}N_k$ individer.

  • Sundhedstjek:

    $$g frac{N_k^2}{N_k+I_k} + g frac{2N_kI_k+I_k^2}{N_k+I_k} = g (N_k+I_k)$$

Model med jordinfektion

Lad os nu tilføje jordinfektionen til modellen. Det betyder simpelthen, at hver generation en anden $frac{30}{1000000}N =: rN$ individer trækkes fra $N$ og lægges til $I$:

$$ egin{alignedat}{3} N_{k+1} &= g frac{N_k^2 }{N_k+I_k} &~-~& rN_k, I_{k+1} &= g frac{2N_kI_k+I_k^2}{N_k+I_k} &~+~& rN_k. end{alignedat} $$

Resultat

Med dette er det nemt at indsætte dine startbetingelser og køre en simulering, her i Python:

# Parametre g = (6070/4)**(1/600) r = 30/1000000 K = 600 # Startbetingelser I = 120 N = 4000000-I # Iterer for k i område(K): N,I = ( g*N**2/(N+I)-r*N, g*(2*N*I+I**2)/(N+I)+r*N ) print(k,N,I)

Det viser, at der ikke er nogen ikke-inficerede individer tilbage efter 600 generationer. Faktisk falder $N$ under 1 efter generation 17.

Om ligevægt

Eller ville vi have en form for dynamisk ligevægt mellem II og NI, hvor (tror jeg) førstnævnte ville dominere stærkt?

Nej, der er ingen mekanisme, der på en eller anden måde favoriserer den ikke-inficerede befolkning. Men dette eksisterer ikke: Den inficerede befolkning vokser lige så hurtigt som den ikke-inficerede af sig selv plus inficerer dele af de ikke-inficeredes afkom. Faktisk, som beskrevet i det andet svar, kan vi se på udviklingen af ​​fraktionen $n$ af ikke-inficerede individer i modellen uden jordinfektion:

$$n_{k+1} ≡ frac{N_{k+1}}{N_{k+1}+I_{k+1}} = frac{g frac{N_k^2}{N_k+I_k }}{g (N_k+I_k)} = venstre( frac{N_k}{N_k+I_k} ight)^2 ≡ n_k^2 $$

Den eneste måde, hvorpå nogle ikke-inficerede individer overlever, er hvis de formerer sig hurtigere end de er inficerede, dvs. hvis: $$g frac{N_k}{N_k+I_k} = g n_k > 1.$$ Siden $lim_{ k→∞}n_k=0,$ dette virker ikke selv med en absurd høj vækstrate.


For mange, mange decimaler er procentdelen af ​​II i befolkningen 100%.

For at besvare dette skal du gøre nogle antagelser om parringsstruktur. Jeg antager, at parring er panmiktisk her for nemheds skyld. Ditto kønsforhold, men jeg antager lige mange M/F (og lige stor risiko for miljøinfektion). Endelig går jeg ud fra, at NI og II har samme risiko for jordbåren infektion (og infektioner til II er simpelthen spildt), snarere end at miljøreservoiret på en eller anden måde opsøger en fast andel af NI'er, hvilket jeg tror nok er det du mente . Jeg anvender også den jorderhvervede infektion til generation 0 her (så de har en chance for at blive smittet, før de parrer sig). Endelig kaldes II og NI mere traditionelt $I$ (for infektiøse) og $S$ (for følsomme) i denne type model, så jeg har fulgt denne konvention nedenfor.

Medmindre jeg mangler noget, gør befolkningsstørrelsen ingen forskel: chancen for, at et barn bliver smittet, afhænger ikke af antallet af børn, og baggrundsraten for miljøsmitte er proportional med befolkningsstørrelsen, så det hele udgår. Jeg vil derfor holde mig til proportioner herfra, hvilket betyder, at $I$ og $S$ er proportioner under, ikke absolutte tal.

Hver generation er andelen af ​​parringer mellem to $I$s $I^2$, mellem to $S$s er $I^2$, og mellem et S og et I er $2·S·I$. Så andelen af ​​Is i den næste generation er $I^2 + 2·I·S$. Eller mere enkelt $1-S^2$.

Så:

  • $S(0) = frac{3.999.850}{4.000.000} = 0,9999625$

  • $S(1) = S(0)^2$

  • $S(2) = S(1)^2$, hvilket er ${S(0)^2}^2$

Mere generelt er $S(n) = {S(0)^2}^n$

Så ved generation 600:

$S(600) = {S(0)^2}^{600}$

$2^{600}$ er et meget stort tal. Så det burde ikke være for overraskende, at alle er inficeret af dette punkt.

Vi kan rode rundt (fagudtryk) med ligningen:

$S(n) = {S(0)^2}^n$

… for at løse (for eksempel) hvor mange generationer der skal til, før 50 % af befolkningen bliver smittet:

$$egin{alignat}{1} 0,5 &= {0,9999625^2}^n log(0,5) &= log(0,9999625) imes2^n frac{log(0,5)}{ log(0.9999625)} &= 2^n log_2left(frac{log(0.5)}{log(0.9999625)} ight) &= n end{alignat}$$

Så 50% af din globale befolkning er inficeret af generation 15, kun 300 år inde i simuleringen.

dog vil nogle få NI-personer stadig danne par med NI-kammerater - i et stykke tid

Sandsynligheden for, at nogen ($S$, eller $I$) parrer sig med et $I$-individ er direkte proportional med $I$-andelen af ​​befolkningen, så chancen for, at dette sker, bliver bare ved med at falde hurtigere og hurtigere.


Vi har nu teknologien til at udvikle vacciner, der spreder sig selv

Michelle D’Urbano

Et KENDT citat, der ofte tilskrives Benjamin Franklin, er "en ounce forebyggelse er et halvt kilo kur værd". Verden er nu ved at opdage omkostningerne ved sit pund af kur mod covid-19. Men hvordan ville en ounce forebyggelse se ud?

For infektionssygdomme, der stammer fra vilde dyr, såsom covid-19, SARS, MERS og Ebola, er en løsning at forhindre overførsel til mennesker i første omgang. For at opnå dette er et vigtigt første skridt at ændre vores adfærd for at reducere kontakten med de vilde dyrearter, der huser sådanne sygdomme.

En komplementær tilgang er at målrette mod de infektiøse agenser, der bærer disse sygdomme, ved at reducere deres udbredelse eller eliminere dem i dyrelivspopulationer. Selvom dette ikke er en ny idé, betyder fremskridt inden for teknologi, at vi kan have en bedre chance for at det lykkes end nogensinde før.

Det klassiske eksempel på dette er rabies: vi vaccinerer hunde og mange vilde kødædere for at undertrykke rabies i disse populationer og dermed reducere vores egen risiko for at fange den. Selvom disse vaccinationskampagner praktisk talt har elimineret menneskelig rabies i USA og Europa, dræber sygdommen stadig mere end 55.000 mennesker årligt i Afrika og Asien, hvor omkostningerne ved vaccinationsprojekter for vilde dyr er en barriere for at opretholde et tilstrækkeligt niveau af immunitet.

Brug af vaccination mod vilde dyr til at målrette mod andre farlige patogener, der cirkulerer i flagermus og gnavere – såsom ebola-, Marburg-, SARS- og Lassa-virus – står over for lignende forhindringer, hvilket forværres af den hurtige befolkningsomsætning og store bestandsstørrelser af disse dyr.

En mulig løsning er at skabe vacciner, der spreder sig gennem en dyrepopulation.

Disse "selvspredningsvacciner" kan udvikles på mindst to måder. Den konventionelle tilgang bygger på at påføre en vaccine på pelsen af ​​fangede dyr og frigive dem. Når disse dyr vender tilbage til deres naturlige hjem, resulterer social pleje i, at vaccinen indtages af andre individer, hvilket forstørrer niveauet af immunitet, der kan opnås.

Dette viser løfte om at reducere truslen om rabies, der overføres til mennesker fra f.eks. vampyrflagermus.

En mere radikal tilgang er afhængig af at indsætte et lille stykke af genomet af infektionssygdomsagenset i en godartet virus, der spredes naturligt gennem dyrepopulationen. Da denne overførbare vaccine spredes fra dyr til dyr, immuniserer den dem mod målinfektionssygdommen, hvilket i høj grad øger immuniteten i dyrepopulationen og reducerer risikoen for afsmitning til mennesker.

Teknologien til at udvikle overførbare vacciner eksisterer nu, og feltforsøg fokuseret på at beskytte vilde kaniner mod en viral hæmoragisk feber ved hjælp af denne teknik har vist lovende resultater. Der arbejdes nu på at udvikle prototyper for flere vigtige menneskelige patogener, såsom Lassa- og Ebola-virus.

Selvspredningsvacciner kunne være en revolutionerende teknologi til at reducere truslen om menneskelige infektionssygdomme, der springer til os fra vilde dyr. Ud over at gøre vaccination til vilde dyr mulig og omkostningseffektiv, reducerer denne teknologi motivationen til at aflive eller udrydde økologisk vigtige sygdomsreservoirarter, såsom flagermus.

Der er dog stadig meget arbejde at gøre. Laboratorie- og feltforsøg skal kontrollere, hvor effektiv denne tilgang er, og se efter mulige uventede konsekvenser af
selvspredningsvacciner. Men efterhånden som omkostningerne ved vores igangværende forsøg på at finde en "kur" mod covid-19 fortsætter med at akkumulere, ser et gram forebyggelse ud til at være en bedre investering for hver dag, der går.

Selvspredningsvacciner til nye infektionssygdomme
https://pubmed.ncbi.nlm.nih.gov/26524478/


Vaccine incitamenter

I løbet af de sidste mange uger er vaccinationstempoet i USA aftaget, og i stigende grad har regeringer og private virksomheder tilbudt incitamenter til vaccination. Det er selvfølgelig ikke overraskende, at vaccinationstempoet ville begynde at falde efter en hurtig start. Det var trods alt dem, der havde mest lyst til at blive vaccineret, dem, der opsøgte vaccinen, selv når den endnu ikke var almindelig tilgængelig, og det tog en del indsats at blive vaccineret. Nu hvor udbuddet af vacciner har indhentet (og overgået) efterspørgslen, er opgaven blevet sværere, og det er ikke kun misinformation om antivaccine, der er årsagen. De personer, der er tilbage til at modtage vaccinen, omfatter de unge (som måske ikke tror, ​​de har brug for det), dem, der ikke har let adgang til vaccinen, såsom de fattige og dem, der har svært ved at tage fri fra arbejde for at blive vaccineret og føler, at de kan. 8217t har råd til at blive sat på sidelinjen af ​​bivirkninger, og ja, vaccinen tøver.

Som følge heraf tilbyder nogle stater og virksomheder incitamenter, som Mercola, som Mercola, ser som en sammensværgelse:

De seneste uger har set en markant stigning i alle slags vaccinationsincitamenter i USA, lige fra gratis doughnuts, kage, 4 pommes frites, hotdogs og pizza, 5 til arkadepoletter, 6 10-cent øl, 7 sæsonkort til frie statsparker, 8 gratis Uber- og Lyft-ture, 9 gratis marihuana 10- og Cincinnati Reds-baseballbilletter, 11 en chance for at vinde et fuldt stipendium 12 og endda $1 million 13 og $5 millioner 14 giveaways.

Nedenfor er en mere komplet liste over incitamenter, offentliggjort på vaccines.gov. 15 Som du kunne forvente, har million-dollar-lotterierne vist sig at være en bragende succes, der krediteres for at lokke millioner af mennesker til at få deres skud. 16

Som bemærket af Ohio’s første “Vax-a-Million” lotterivinder”, var chancen for en vinder for stor til at modstå. “Jeg blev ved med at hæve og tude om det, og jeg arbejder hele tiden, og da Vax-a-Million-tinget startede, gik jeg straks derned og fik det. Det skubbede mig ud over kanten,” sagde han til en lokal avis. 17

Det ville være en dybt alvorlig underdrivelse at sige, at vaccinepresset har en luft af desperation.

Jeg vil indrømme, at jeg er lidt urolig over nogle af incitamentsprogrammerne, såsom million-plus-dollar-lotteriet. Når det er sagt, ser det ud til, at incitamenterne virker til en vis grad, da vaccinationsraten for nylig er begyndt at komme sig efter krateret for en måned siden, og det ser ud til, at incitamenterne er kommet for at blive, i hvert fald indtil vaccinationsraten når en højt nok punkt til at forhindre store udbrud og fornyede stigninger.

Det er ikke overraskende, at Mercola gentager gambiten og påberåber sig databasen Vaccine Adverse Events Reporting System (VAERS) for at hævde, at COVID-19-vacciner er dødelige. Jeg har allerede skrevet om det særlige vildledende trick, senest sidste gang jeg diskuterede McCullough, men også i januar og februar. Jeg hentydede endda til det så langt tilbage som i december. Så ukarakteristisk vil jeg ikke gå (meget) ind i det spil her, bortset fra at nævne, at Mercola også fremfører løgnen om, at vaccinerne er “eksperimentel genterapi“.

Så hvad er det ifølge Mercola og McCullough ægte grunden til, at myndighederne ønsker høje niveauer af vaccination mod COVID-19? De ønsker at “affolke” verden. Nej, jeg laver ikke sjov:

Hvorfor bliver vaccinen skubbet på denne måde? McCollough mener, at det er et globalt mål at “mark” mennesker, at få dig ind i deres vaccinedatabase, som i sidste ende vil blive omdannet til et værktøj til befolkningskontrol, takket være vaccinepas.

Når vi taler om befolkningskontrol, er der to forskellige former, og begge kan være gældende i dette tilfælde. En form for befolkningskontrol handler om at kontrollere mennesker gennem ideologien om utilitarisme, vaccinepas og et socialt kreditsystem, som alle er bundet sammen. En anden form er egentlig affolkning.

Selvfølgelig er dette også en gammel antivaccine-konspirationsteori, der er genbrugt til COVID-19-vacciner. Faktisk skrev jeg om dette i det mindste for ni år siden, da antivaccine-konspirationsteoretikeren John Rappaport i det væsentlige skrev det samme om H1N1-vaccinen, nemlig at det var et plot om at affolke verden. Jeg vil henvise tilbage til Rappaports artikel, efter at jeg har set på Mercola og McCulloughs påstande.


SIR-modellen for spredning af sygdom - Differentialligningsmodellen

Som det første trin i modelleringsprocessen identificerer vi de uafhængige og afhængige variable. Den uafhængige variabel er tid  t,  målt i dage. Vi betragter to relaterede sæt af afhængige variable.

Det første sæt af afhængige variable tæller mennesker i hver af grupperne, hver som en funktion af tiden:

S = S(t) er antallet af modtagelige enkeltpersoner,
I = I(t) er antallet af inficeret enkeltpersoner, og
R = R(t) er antallet af genvundet enkeltpersoner.

Det andet sæt af afhængige variabler repræsenterer brøkdel af den samlede befolkning i hver af de tre kategorier. Så hvis  N  er den samlede befolkning (7.900.000 i vores eksempel), vi har

s(t) = S(t)/N, den modtagelige del af befolkningen,
i(t) = I(t)/N, den inficerede del af befolkningen, og
r(t) = R(t)/N, den genvundne del af befolkningen.

Det kan virke mere naturligt at arbejde med befolkningstællinger, men nogle af vores beregninger bliver enklere, hvis vi i stedet bruger brøkerne. De to sæt afhængige variabler er proportionale med hinanden, så begge sæt vil give os den samme information om epidemiens fremskridt.

    Under de antagelser, vi har gjort, hvordan tænker du  s(t)  bør variere med tiden? Hvordan skal  r(t)  variere med tiden? Hvordan skal  det)  variere med tiden?

Dernæst foretager vi nogle antagelser om ændringshastighederne for vores afhængige variable:

Ingen er tilføjet til den modtagelige gruppe, da vi ignorerer fødsler og immigration. Den eneste måde et individ blade den modtagelige gruppe er ved at blive smittet. Vi antager, at ændringshastigheden på  S(t),  den nummer af modtagelige, 1 afhænger af antallet, der allerede er modtagelige, antallet af individer, der allerede er inficeret, og mængden af ​​kontakt mellem modtagelige og inficerede. Antag især, at hvert inficeret individ har et fast nummer  b  af kontakter om dagen, der er tilstrækkelige til at sprede sygdommen. Ikke alle disse kontakter er med modtagelige personer. Hvis vi antager en homogen sammenblanding af befolkningen, vil de brøkdel af disse kontakter, der er med modtagelige, er  s(t).  Således genererer hvert inficeret individ i gennemsnit  b s(t)  nye inficerede individer om dagen. [Med en stor modtagelig befolkning og en relativt lille inficeret befolkning, kan vi ignorere vanskelige tællesituationer, såsom en enkelt modtagelig, der støder på mere end én inficeret på en given dag.]

Lad os se, hvad disse antagelser fortæller os om derivater af vores afhængige variable.

    Den modtagelige ligning . Forklar omhyggeligt, hvordan hver komponent i differentialligningen

(1)

følger af teksten forud for dette trin. I særdeleshed,

    Hvorfor er faktoren  Det)  til stede?

(3)

følger af en af ​​antagelserne forud for trin 4.

(4)

Hvilken antagelse om modellen afspejler dette? Forklar nu omhyggeligt, hvordan hver komponent i ligningen

(5)

følger af hvad du har gjort indtil nu. I særdeleshed,

Til sidst afslutter vi vores model ved at give hver differentialligning en startbetingelse. For denne særlige virus - Hong Kong-influenza i New York City i slutningen af ​​1960'erne - var næsten ingen immune i begyndelsen af ​​epidemien, så næsten alle var modtagelige. Vi vil antage, at der var et spor af infektion i befolkningen, f.eks. 10 personer. 2  Således er vores begyndelsesværdier for populationsvariablerne

S(0) =ه.900.000
I(0) =㺊
R(0) =ـ

Med hensyn til de skalerede variabler er disse startbetingelser

s(0) =ف
i(0) =ف.27 x㺊 - 6
r(0) =ـ

(Bemærk: Summen af ​​vores startpopulationer er ikke nøjagtigt  N,  er heller ikke summen af ​​vores brøker nøjagtigt  1.  Sporniveauet af infektion er så lille, at dette ikke vil gøre nogen forskel.) Vores komplette model er

Vi kender ikke værdier for parametrene  b  og    endnu, men vi kan estimere dem og derefter justere dem efter behov for at passe til de overskydende dødsdata. Vi har allerede estimeret den gennemsnitlige smitteperiode til tre dage, så det tyder på  k =ف/3.  Hvis vi gætter på, at hver inficeret ville få en muligvis inficerende kontakt hver anden dag, så  b  ville være  1/2.  Vi understreger, at dette kun er et gæt. Følgende plot viser løsningskurverne for disse valg af  b  og  k

    I trin 1 og 2 noterede du dine ideer om, hvordan løsningsfunktionerne skulle se ud. Hvordan er disse ideer sammenlignet med figuren ovenfor? I særdeleshed,

    Hvad synes du om det relativt lave niveau af infektion på toppen af ​​epidemien?

I del 3 vil vi se, hvordan løsningskurver kan beregnes selv uden formler for løsningsfunktionerne.

1  Bemærk, at vi har forvandlet adjektivet "modtagelig" til et substantiv. Det er almindelig brug inden for epidemiologi at henvise til "modtagelige", "smittede" og "frivillige" i stedet for altid at bruge længere sætninger som "befolkning af modtagelige mennesker" eller endda "den modtagelige gruppe."

2  Mens jeg (0) er normalt lille i forhold til N, skal vi have I(0) >ـ for at udvikle en epidemi. Ligning (5) siger ganske rimeligt, at hvis Jeg =ـ på tidspunktet 0 (eller når som helst), så dI/dt =ـ så godt, og der kan aldrig komme nogen stigning fra 0 niveau af infektion.

David Smith og Lang Moore, "SIR-modellen for spredning af sygdom - differentialligningsmodellen," Konvergens (december 2004)


Faktorer i opkomsten eller genfremkomsten af ​​infektionssygdomme

Der er mange faktorer involveret i fremkomsten af ​​nye infektionssygdomme eller genfremkomsten af ​​"gamle" infektionssygdomme. Nogle er et resultat af naturlige processer såsom udviklingen af ​​patogener over tid, men mange er et resultat af menneskelig adfærd og praksis. Overvej, hvordan samspillet mellem den menneskelige befolkning og vores miljø har ændret sig, især i det sidste århundrede. Faktorer, der har bidraget til disse ændringer, er befolkningstilvækst, migration fra landdistrikter til byer, internationale flyrejser, fattigdom, krige og ødelæggende økologiske ændringer som følge af økonomisk udvikling og arealanvendelse.

For at en ny sygdom kan etablere sig skal der indtræffe mindst to hændelser – (1) det smitsomme agens skal introduceres i en sårbar befolkning, og (2) agensen skal have evnen til at sprede sig let fra person til person og forårsage sygdom. Smitten skal også kunne opretholde sig selv i befolkningen, det vil sige, at flere og flere bliver ved med at blive smittet.

Mange nye sygdomme opstår, når smitsomme stoffer i dyr overføres til mennesker (benævnt zoonoser). Efterhånden som den menneskelige befolkning udvides i antal og ind i nye geografiske områder, øges muligheden for, at mennesker vil komme i tæt kontakt med dyrearter, der er potentielle værter for et smitsomt agens. Når denne faktor kombineres med stigninger i menneskets tæthed og mobilitet, er det let at se, at denne kombination udgør en alvorlig trussel mod menneskers sundhed.

Klimaændringer bliver i stigende grad en bekymring som en faktor i fremkomsten af ​​infektionssygdomme. Efterhånden som jordens klima opvarmes og levesteder ændres, kan sygdomme spredes til nye geografiske områder. For eksempel tillader opvarmende temperaturer myg - og de sygdomme, de overfører - at udvide deres rækkevidde til områder, hvor de ikke tidligere er blevet fundet.

En faktor, der er særlig vigtig ved genopkomsten af ​​sygdomme, er antimikrobiel resistens – patogeners erhvervede resistens over for antimikrobielle lægemidler som f.eks. antibiotika. Bakterier, vira og andre mikroorganismer kan ændre sig over tid og udvikle en resistens over for de lægemidler, der bruges til at behandle sygdomme forårsaget af patogenerne. Derfor er lægemidler, der var effektive i fortiden, ikke længere nyttige til at kontrollere sygdom.

En anden faktor, der kan få en sygdom til at dukke op igen, er et fald i vaccinedækningen, så selv når der findes en sikker og effektiv vaccine, vælger et stigende antal mennesker ikke at blive vaccineret. Dette har været et særligt problem med mæslingevaccinen. Mæslinger, en meget smitsom og alvorlig infektion, der blev elimineret fra USA i 2000 og fra den vestlige halvkugle i 2016, er vendt tilbage i visse områder på grund af en stigning i antallet af mennesker, der vælger at tage ikke-medicinske vaccinefritagelser af personlige og filosofiske årsager tro. Dette er blevet drevet af en anti-vaccinebevægelse, der i vid udstrækning var baseret på en ugyldig og miskrediteret undersøgelse, der hævdede en sammenhæng mellem en vaccine mod mæslinger og autisme. Som et resultat af faldet i vaccinedækningen er mæslingetilfældene det højeste i dette årti med mere end 1.000 tilfælde af mæslinger rapporteret i USA i første halvdel af 2019.


Coronavirus 2.0 kan være op til NI GANGE mere smitsom ... men det kan være grund til at fejre

Nyheden kommer fra forskning offentliggjort i denne uge i det amerikanske videnskabelige tidsskrift &lsquoCell&rsquo. Det involverede genetisk sekventering af mere end 6.000 coronavirus DNA-sekvenser indsamlet fra hele verden. Af alle disse tusindvis af varianter var en, der gjorde forskerne særligt bekymrede, Spike D614G-stammen &ndash en mutantvirus med en afgørende ændring i dens DNA-kode, der påvirker de såkaldte &lsquospike-proteiner&rsquo på virusets overflade. Disse pigge er det, der tillader den at trænge ind i menneskelige celler, og mutationen ser ud til at gøre den endnu bedre til at gøre det.

En foreløbig version af disse resultater var allerede blevet offentliggjort på preprint-depotet med åben adgang bioRxiv forud for en peer review som &ldquoan tidlig advarsel&rdquo til andre forskere, der studerer nye virusstammer. Men siden da har forskerne bag undersøgelsen bekræftet, at den nye stamme ikke er forbundet med &ldquo øget sygdoms sværhedsgrad.&rdquo Med andre ord, det gør folk mere syge end de tidligere stammer, der oprindeligt spredte sig i Europa og Amerika.

Champagne, nogen?

Så hvorfor er dette gode nyheder? Handler alt, hvad vi hører fra politikere, embedsmænd i folkesundheden og de almindelige medier om, hvordan vi skal bremse, stoppe og endda knuse spredningen af ​​virussen? De har alle sunget fra det samme salmeark på dette budskab i flere måneder nu. Men der er et lille problem: de har en anelse om, hvad de taler om.

Igen skal opmærksomheden her henledes på det grundlæggende princip, der styrer livscyklussen for en respiratorisk virus: en vellykket virus er en mild virus. En vært, der er alvorligt svækket eller død, kan ikke sprede virussen gennem hoste og nys. Efterhånden som virussen replikerer og udvikler sig, vil mutationer, der har tendens til at gøre den mildere (og derfor mindre dødelig), have tendens til at opbygge sig i de mest udbredte stammer.

Gudskelov er dette ikke en anden slags virus, såsom ebola, som på én gang kan være dødelig og smitsom, fordi den spredes gennem kropsvæsker. En respiratorisk virus kan kun være den ene eller den anden (eller et sted på spektret derimellem).

Hvis du ikke tror mig, hvad med at trække på ekspertisen fra Lawrence Young, en professor i molekylær onkologi ved University of Warwick. Han var ikke involveret i undersøgelsen, så han havde ingen egeninteresse. Han fortalte CNN: &ldquoDet nuværende arbejde tyder på, at selvom Spike D614G-varianten kan være mere smitsom, er den ikke mere patogen. Der er et håb om, at efterhånden som SARS-CoV-2-infektionen spredes, kan virussen blive mindre patogen.&rdquo

Eller hvad med Edward Feil, professor i biologi og biokemi ved University of Bath. Han skriver i The Spectator i fredags og forklarer, hvordan det ikke er muligt at forudsige den fremtidige spredning af en virus - selv en aktiv, hvor DNA-sekvensen er kendt: &ldquoDet er næsten umuligt at forudsige fremtidige baner for virulens og overførsel af nye patogener.&rdquo Han begynder dog med at citere den almindelige visdom, som enhver kompetent biologistuderende bør kende: &ldquoet nyt patogen [&hellip] vil udvikle sig over tid for at blive mere godartet og leve i venskab med sin vært.&rdquo Det er præcis, hvad Spike D614G repræsenterer.

Hurtigere, virus! Spredning! Spredning!

Hvor sikker er jeg på, at spredning af virussen faktisk er bedre for folkesundheden end ikke at sprede den? Ikke 100 procent sikker, men en helvedes meget mere sikker end politikerne og de højtlønnede embedsmænd i hælene, så sjældent fraværende fra vores tv-skærme i disse dage.

Hvad angår den anden bølge af viden, en idé så attraktiv og ubegrundet som en enhjørning, vil denne nyhed give mere opmuntring til troende. Selvfølgelig kan en mere virulent stamme meget vel føre til flere tilfælde af virussen &ndash, selvom som præsident Trump sagde så klogt forleden: &ldquoHvis vi holder op med at teste lige nu, har vi faktisk meget få tilfælde.&rdquo Dette førte til et mindre mediehyseanfald, men Trump havde bogstaveligt talt ret i den forstand, at sagerne ikke ville blive identificeret.

Hvis Trump ikke er din taske, hvad med at følge ledelsen af ​​Sunetra Gupta, professor i teoretisk epidemiologi ved University of Oxford og en hovedforfatter af &lsquoOxford-modellen&rsquo. Dette var et forudseende og fornuftigt alternativ til Neil Fergusons Imperial College London-model om Covid-19, som forudsagde en halv million britiske dødsfald. Oxford-modellen redegjorde for det faktum, at virussen kan have spredt sig frit i hele befolkningen, før lockdowns blev pålagt, hvilket gjorde dem meningsløse.

Ifølge professor Gupta er dødsfald, og ikke tilfælde &ldquote den eneste pålidelige foranstaltning.&rdquo Og hvis der er en anden bølge af dødsfald, begynder jeg at tro på enhjørninger.

Tror du, at dine venner ville være interesserede? Del denne historie!

Udtalelserne, synspunkterne og meningerne i denne kolonne er udelukkende forfatterens og repræsenterer ikke nødvendigvis RTs.


Referencer (dette afsnit)

  1. Centre for Disease Control and Prevention. Hepatitis A-udbrud forbundet med grønne løg på en restaurant&ndashMonaca, Pennsylvania, 2003. MMWR 2003 52(47):1155&ndash7.
  1. Cobb S, Miller M, Wald N. Om estimering af inkubationsperioden ved malign sygdom. J Chron Dis 19599:385&ndash93.
  1. Kelsey JL, Thompson WD, Evans AS. Metoder i observationsepidemiologi. New York: Oxford University Press 1986. s. 216.
  2. Lee LA, Ostroff SM, McGee HB, Jonson DR, Downes FP, Cameron DN, et al. A. udbrud af shigellose ved en udendørs musikfestival. Am J Epidemiol 1991. 133:608&ndash15.
  3. White DJ, Chang H-G, Benach JL, Bosler EM, Meldrum SC. Betyder RG, et al. Geografisk spredning og tidsmæssig stigning af Lyme-sygdomme. epidemi. JAMA 1991266:1230&ndash6.
  4. Centre for Disease Control and Prevention. Udbrud af West Nile-lignende viral encephalitis&ndashNew York, 1999. MMWR 199948(38):845&ndash9.
  5. Centre for Disease Control and Prevention. Forekomst af overvægt og fedme blandt voksne med diagnosticeret diabetes & mdash USA. 1988&ndash1994 og 1999&ndash2002. MMWR 200453(45):1066&ndash8.
  6. Nationalt Center for Sundhedsstatistik [Internet]. Atlanta: Centers for Disease Control and Prevention [opdateret 8. februar 2005]. Tilgængelig fra: https://www.cdc.gov/nchs/products/pubs/pubd/hestats/overwght99.htm.

Figur 1.21

Beskrivelse: Epidemisk kurve (histogram) viser det formodede indekstilfælde af hepatitis A, efterfulgt 4 dage senere af en stejl stigning i tilfælde, som aftager til 0. Tilfælde, der var fødevarebehandlere, og sekundære tilfælde er også vist. Vend tilbage til tekst.

Figur 1.22

Beskrivelse: Histogram viser antallet af tilfælde af diarré efter debutdato. Arrows also show when water main breaks, a boil water order, and water chlorination occur. Bloody and nonbloody diarrheal illness is indicated by different colors. Overall increases and decreases in cases is easily seen. Return to text.

Figure 1.23

Beskrivelse: Histogram shows the number of measles cases peaks around November 23 then declines. It peaks again on December 5 and declines until it peaks a third time. Return to text.

Figure 1.24

Beskrivelse: Histogram shows the number of Shigella cases among staff and attendees in stacked bars. The first case occurs in a staff member on day 1. The number of cases among staff and attendees is seen in relationship to the festival dates. Return to text.

Figure 1.25

Beskrivelse: Histogram shows a general increasing trend in the number of reported cases of Lyme disease. Return to text.

Figure 1.26

Beskrivelse: Histogram shows reported cases of West Nile Encephalitis in New York City and other locations. In NYC, cases drop to 0 after mosquito control activities are begun in the city. Reported cases in other locations continue at about the same rate. Return to text.


The SARS-CoV-2 virus that causes the disease COVID-19 is nimbly and stealthily racing through community after community devastating the world’s population. Over 23 million people have contracted the virus worldwide and 810,000 have died. It is critical to review the evolutionary history of this particular virus to provide necessary insights into how the pandemic can be brought under control.

Researchers worldwide are working arduously to trace the virus globally by studying samples obtained from various nations looking for subtle mutations that it undergoes as it infects, replicates and multiplies, providing them clues to the source and route of spread.

COVID-19 is caused by a type of coronavirus known as SARS-CoV-2, named for its similarity to the coronavirus that caused SARS. The virus is called a coronavirus because it is covered by club-like structures that give the virus a similar look to the sun’s corona in electron micrographs.

The SARS-CoV-2 virus is part of a family of organisms that are known to infect mammals and birds. Det Coronaviridae family are made up of a positive-sense single-stranded RNA completely enveloped in a complex protein and bilipid shell. These viruses are relatively large, consisting of 26 to 32 kilobase pairs. RNA or ribonucleic acid is a nucleic acid that is essential for all reproductive processes and like DNA.

The first known scientific encounter with this family of virus is thought to be when veterinarians puzzled over bronchial infections afflicting cats, pigs, and chickens in the early 20th century.

Study of disease afflicting and damaging tobacco crops in the late 19th century led some thoughtful scientists like Dimitri Ivanovsky to conjecture the existence of non-bacterial infectious agents causing the “tobacco mosaic disease.” It would take another 50 years to capture the first images of the Tobacco Mosaic Virus. The invention of the electron microscope in 1931 enabled scientists to observe viruses more closely, allowing a more extensive and direct study of these micro-organisms. Virology as a field began to flourish.

Human coronaviruses were first identified in the 1960s. Seven species of coronavirus are known to afflict humans. Four result in relatively mild upper respiratory tract conditions, including the virus 229E that causes the common cold, along with NL63, OC43 and HKU1.

The other three strains, SARS, MERS, and SARS-CoV-2, are far more virulent. All these viruses were new to human populations when they first arose in the 21st century. A feature of SARS, MERS and COVID-19 is that they had a zoonotic origin, that is they originated in animal populations and then jumped into humans. The SARS outbreak in 2002, with a case fatality rate of 11 percent, showed the world the deadly potential of coronaviruses, but this was a warning that was mostly ignored. There had only been 8,422 cases and since 2004 no SARS-CoV has been reported worldwide. One advantage for public health responses to SARS was that it had an incubation period of 4 to 6 days and patients presented with symptoms prior to becoming infectious.

In their extensive investigations, the World Health Organisation (WHO) concluded that the SARS virus originated in bat populations, but the exact species remains unknown. Work commenced on the development of a SARS vaccine with testing on animals. The vaccine resulted in protective immunity but produced an immune mediated hypersensitivity as an adverse effect. The SARS threat, for unknown reasons, expired after six months though limited outbreaks did occur later.

With the threat of a pandemic having ended after six months, so did any interest in funding a vaccine, as pharmaceutical companies saw no profit in funding or exploring such research. The co-director of the Center for Vaccine Development at Texas Children’s Hospital and dean of the National School of Tropical Medicine at the Baylor College of Medicine in Houston, Dr. Peter Hotez, had been attempting to develop a SARS vaccine in 2016 but couldn’t get funding for his work. “We tried like heck to see if we could get investors or grants to move this into the clinic . But we just could not generate much interest,” he said.

“We could have had this ready to go and been testing the vaccine’s efficacy at the start of this new outbreak in China (COVID-19) … There is a problem with the ecosystem in vaccine development, and we’ve got to fix this,” Hotez said.

The genomic sequence of the SARS virus was published in August 2003 by Chinese scientists in Beijing. In actuality, when the cause of the pneumonia-like illness was first identified in Wuhan, some believed this was a new outbreak of the SARS virus. SARS-CoV-2 and SARS share a genomic sequence that is approximately an 80 percent match.

Middle East Respiratory Syndrome, or MERS, emerged in Saudi Arabia in 2012 and had a zoonotic origin in bats and was spread to humans through contact with dromedary camels. The virus produced symptoms similar to SARS but it had a low infectivity though highly lethal. Of the reported 2,500 cases, 35 percent died from the disease.

With limited capacity to spread from human to human, it was mainly passed through contact with infected people in hospitals. In the main it was concentrated in the Arabian Peninsula, although there were further outbreaks in South Korea in 2015 and Saudi Arabia in 2018. It continues to smoulder in the Middle East.

When the SARS CoV-2 virus emerged in late 2019, the world was totally unprepared. Health systems internationally had been systematically run down and were ill-equipped to respond. The warnings from WHO of the dangerous potential of the virus were largely ignored or belittled. The murderous government policies that dominated have been described as malign neglect or herd immunity.

SARS CoV-2 arose in Wuhan in December 2019. The virus is thought to have originated from bats and to have transferred to humans through an intermediary species. The exact origins of the virus may never be known. “It is quite possible we won’t find it (the species). In fact, it would be exceptionally lucky if we land on something,” a geneticist from University College London, Lucy van Dorp, told Natur .

Back in 2013, the Wuhan Institute of Virology had investigated the coronavirus genome from the horseshoe bat ( Rhinolophus affinis ). The viruses named RATG13 and SARS-CoV-2 were found to be 96 percent genetically similar. There are, however, subtle molecular changes that continue to be investigated that contribute to selection pressures that drive the virulence, pathogenicity, and immunogenic qualities of the virus.

In their detailed analysis of the origin of the SARS-CoV-2 virus, Andersen et al., 2020, offered three possible explanations: 1) natural selection in an animal host before jumping into humans, 2) natural selection in humans after the virus transferred into human hosts, and 3) the product of artificial manipulation, which has been refuted by several virologists. According to Van Dorp, “… the 4% difference between the genomes of SARS-CoV-2 and RATG13 still represents some 50 years since they last shared a common ancestor.”

It was thought that pangolins ( Manis javanica ), a scaly ant-eating mammal, may be the intermediate host between bats and humans, but genetic studies indicate that as unlikely. However, some scientists think that because coronavirus-like SARS-CoV-2 cases have been found in pangolins, that species cannot be ruled out as the intermediary source.

Scientists are currently examining species of animals that were kept and sold in the live markets in Wuhan where bats may have been in the buildings’ roof near animals and humans. Presently a team of experts from the WHO are working with their Chinese counterparts to answer this pressing question.

“The opportunities for these viruses to spill over across a very active wildlife-livestock-human interface is clear and obvious,” the president of the EcoHealth Alliance in New York City, Peter Daszak, told Natur. The complex evolutionary history of SARS-CoV-2 disproves President Donald Trump’s ignorant claims (which have a political purpose) that the virus came out of a Chinese laboratory. “Whether they [China] made a mistake, or whether it started off as a mistake and then they made another one, or did somebody do something on purpose?” Trump said.

In a recent paper published in Naturens mikrobiologi —“Evolutionary origins of the SARS-CoV-2 sarbecovirus lineage responsible for the covid-19 pandemic,” led by Maciej F Boni from the Center for Infectious Disease Dynamics at Pennsylvania State University—found that the lineage of SARS-CoV-2 had been circulating in bat populations for decades. “If these viruses have been around for decades that means that they’ve had lots of opportunity to find new host species, including humans,” said Professor David Robertson from the University of Glasgow.

Scientists have carefully examined the Receptor Binding Domain (RBD) of the genetic sequence that codes for the spike protein, the necessary structure on the virus’ exterior shell that is used to bind and penetrate the human cell. The spike protein has been compared to a grappling hook that grips the host cell, then creates a cleavage site that enables the opening and penetration into the host cell.

This means that the SARS-CoV-2 spike proteins had evolved to target a feature of human cells known as angiotensin converting enzyme 2 receptor (ACE2) which are well known to assist in regulating blood pressure.

Andersen et al ., remark that the RBD is the critical component of the spike protein that allows it to bind to ACE2 receptors. SARS-CoV-2 appears to bind with great affinity to the human ACE2 receptors, but computational analysis predicted that the interaction is not ideal. Ifølge New York Times, “the authors indicate that the high-affinity bindings of the virus’ spike protein to human ACE2 is most likely a by-product of natural selection that has permitted another ‘optimal binding solution to arise.’ They then conclude that this is strong evidence that SARS-CoV-2 is not a product of genetic reconstruction or tampering.”

“These two features of the virus, the mutations in the RBD portion of the spike protein and its distinct backbone, rule out laboratory manipulation as a potential origin for SARS-CoV-2,” wrote Kristian Andersen, associate professor of immunology and microbiology at Scripps Research, and co-leader of the study.

With SARS-CoV-2 virus proliferating around the world, the opportunity arises for further mutations and the emergence of new strains of the virus. This can mean that new virus strains may develop in the future not treatable by possible vaccines that were originally made to treat older strains.

According to Assistant Teaching Professor of Computer Science and Technology Niema Moshiri, COVID-19’s mutation rate is lower than seasonal influenza. The SARS-CoV-2 genome has a limited repair function that edits out most mutations. This has meant the virus has remained relatively uniform.

“What we are finding is that the SARS-CoV-2 virus appears to be mutating more slowly than the seasonal flu which may allow scientists to develop a vaccine,” Moshiri wrote on LiveScience. Despite this, variations do occur, and virologists are constantly looking at the variants to determine if a more virulent strain may be emerging or if the virus is losing its potency.

Scientists are collecting virus sequences and storing them in a globally available database. This is used to determine the rate of mutation and where in the virus genome mutations are occurring. Such mutations can affect the virulence and how effectively the virus can infect human host cells. The existence of different viral strains can be used to trace outbreaks.

Analysis of the SARS-CoV-2 virus from different countries has shown that the virus has undergone several predicted but insignificant mutations already. Scientists led by Peter Forster, along with researchers based in the UK and Germany, traced 160 COVID-19 genomes from China, Europe, and the US. They identified three strains of the virus called A, B and C. Type A is considered to be the original Chinese “ancestral type.” Type B is found in Asia, Europe and the US and has diverged from A with 2 mutations. Type C differs from type B at one site and is mostly confined to Europe and mostly absent from China.

More recently, researchers have alerted that a new strain, D614G, has become dominant in many countries. “The D614G variant first came to our attention in early April, as we had observed a strikingly repetitive pattern. All over the world, even when local epidemics had many cases of the original form circulating, soon after the D614G variant was introduced into a region it became the prevalent form,” wrote theoretical biologist at Los Alamos National Laboratory Bette Korber, in the journal Celle .

“This mutation is present in roughly two third of all global strains,” according to Associate Professor Denis Bauer, transformational bioinformatics team leader at CSIRO’s Australian e-Health Research Centre. The mutation that originated in the virus’ spike protein (not the RBD section) is thought to make it more contagious, but speculation that the virus is more virulent is extremely difficult to prove.

Scientists from the Department of Epidemiology of Microbial Diseases at the Yale School of Public Health led by Nathan D. Grubaugh published a paper in Celle titled “Making Sense of Mutation: What D614G Means for the COVID-19 Pandemic Remains Unclear.” The paper examines whether the strain is more transmissible, infectious, or deadly, but concludes that “these data do not prove that G614 is more infectious or transmissible than viruses containing D614.” They conclude there is no evidence that the virus strain leads “to more severe disease.”

The history of human populations and coronaviruses indicate a possible course for the current pandemic. For instance, the virus OC43 is responsible for the common cold, but a study by researchers from the University of Leuven in Belgium suggest it may have been responsible for a pandemic in 1889 that killed more than 1 million people internationally. They speculate that humans eventually developed immunity against the virus, making future infections more benign.

The course of this pandemic is on par with one of history’s most severe health crisis in modern times. For humanity to develop herd immunity to SARS-CoV-2 would imply untold millions of deaths and incompletely understood chronic health morbidities. Yet, in the 21st century, where scientific knowledge is capable with confronting the threat, capitalism enchains humanity’s ability to respond in kind.


Implications for agriculture

Enhancing the resistance of farm animals to infectious disease is an aspiration of veterinary medicine and most agricultural industries, not least because intensive farming is only possible if infectious diseases can be controlled. Traditional selective breeding, genetic engineering, and immunization can all be used to make animals more resistant to infections. If pathogens in nature respond to increases in host resistance by evolving greater virulence, however, is it possible that such efforts will unintentionally select for the same response in pathogens infecting farm animals?

Nothing will happen if hosts are made completely resistant: stop onward transmission, and evolution will cease as well. But artificially enhanced resistance is often imperfect. Many vaccines used on farms do not render hosts impervious to infection, and animal breeders have yet to produce animals completely resistant to a number of different infections. In those situations, pathogens will evolve in newly resistant hosts, just as MYXV, RHDV, WNV, and MG did. Given what we now know about pathogen-host arms races, we think we have to take seriously the possibility that by creating resistant hosts, humans might trigger the evolution of more-virulent animal pathogens.

In fact, this may have already happened. Marek’s disease virus (MDV) is a highly contagious cancer-causing herpesvirus of poultry. Fenner-style common garden experiments clearly show that MDV has become more virulent over the last 50 years. 10 When the poultry industry began to ramp up in the 1950s, MDV caused mild disease and had little economic impact. Currently, MDV strains that kill all unvaccinated birds in just 10 days are common in the US and Europe. Birds have to be vaccinated or the losses are devastating. Critically, and for reasons not fully understood, MDV vaccines protect against disease but they do not generate so-called sterilizing immunity: vaccinated hosts can become infected and transmit viruses to other chickens.

The best bird would be one that dropped dead as fast as possible, before it has started transmitting virus to other birds.

In a series of experiments with strains of varying virulence, one of us (AR), together with Venu Nair and colleagues at the Pirbright Institute in England, found that the hypervirulent, or “hot,” strains of MDV that dominate nowadays can exist only in vaccinated flocks. In unvaccinated birds, they kill before they have a chance to be transmitted. Vaccines keep birds infected with the hot strains alive and so massively increase their transmission potential. 11 We can’t know for sure that vaccination caused the evolution of the hot strains in the first place (sadly, no Fenner-equivalent experiments tracked the initial evolution), but we can say that without vaccination, there would be no hot strains: vaccination creates the conditions for hot strains to emerge and persist.

We can’t help but wonder if something similar is happening in other poultry diseases. Highly pathogenic strains of several viruses—most notably, those that cause infectious bursal disease, avian influenza, and Newcastle disease—arise from circulating strains that are less virulent. The resulting outbreaks can be economically devastating. In all those cases, vaccines are available and often widely used. But none of the vaccines generate sterilizing immunity. We think it should be a top priority to determine whether, by reducing bird fatalities and hence the death rates of hypervirulent strains, vaccines are actually increasing the risk of outbreaks of highly pathogenic avian influenza in birds.

In addition to vaccination, breeding companies that raise poultry and other livestock often try to use selective breeding to enhance resistance. For example, particular major histocompatibility complex alleles in poultry reduce the severity of disease caused by Marek’s disease virus, and there are concerted efforts to spread those alleles through national flocks. This breeding, as well as the increasing development of genetically engineered resistance, 12 may further encourage the evolution and spread of virulent strains. For instance, transgenic chickens have recently been constructed that suppress the replication and transmission of avian influenza, but don’t block it entirely. 13 This is directly analogous to the antiviral effects of MYXV resistance that arose in Australia’s rabbits. Were such chickens to go into widespread use, it is easy to imagine that, just like the rabbits in Australia, they would cause the evolution of more-virulent viruses.

Our suggestion is that breeders and engineers try to do the reverse: breed for susceptibility. The best bird would be one that dropped dead as fast as possible, before it has started transmitting virus to other birds. If death can’t be arranged, engineer an animal that becomes obvious to a farmer on first infection—perhaps something as dramatic as a change of color, which could be monitored by cameras—so it can be removed from the flock before it starts an outbreak. Convincing the industry to employ such a counterintuitive strategy will undoubtedly be difficult, of course.

Moreover, virulence is defined in a standardized host, often one that is fully susceptible. If industrial animals are made more resistant, it may not matter if pathogens become more virulent in response. The threat only exists for those animals that remain susceptible.

For example, there is absolutely no question that MDV has become substantially more virulent over the last 50 years, but industry losses to Marek’s disease are nothing like they were when less virulent strains circulated. 14 One reason is that in vaccinated birds, even today’s hypervirulent strains cause less-severe disease than did milder strains in unprotected birds. Current viral strains only cause problems when they get into unvaccinated flocks—for example, some organic operations, small outdoor flocks, or production systems with faulty vaccination practices. And that’s the rub.

This issue may be of particular concern when it comes to aquaculture, where not all operations in a particular watershed might have access to vaccines or genetically resistant fish stock, and nearby wild populations might be very vulnerable. 15 Likewise, it is easy to envisage non-GMO poultry operations being threatened by hypervirulent pathogens evolving in flocks engineered for resistance. An ethically challenging possibility is that companies deploying resistance-enhancing technologies might gain twice: protection for their own animals and the creation of pathogens that could put their competitors out of business.


‘The Purge’ by Big Tech targets conservatives, including us

Just when we thought the Covid-19 lockdowns were ending and our ability to stay afloat was improving, censorship reared its ugly head.

For the last few months, NOQ Report, Conservative Playbook, and the American Conservative Movement have appealed to our readers for assistance in staying afloat through Covid-19 lockdowns. The downturn in the economy has limited our ability to generate proper ad revenue just as our traffic was skyrocketing. We had our first sustained stretch of three months with over a million visitors in November, December, and January, but February saw a dip.

It wasn’t just the shortened month. We expected that. We also expected the continuation of dropping traffic from “woke” Big Tech companies like Google, Facebook, and Twitter, but it has actually been much worse than anticipated. Our Twitter account was banned. Both of our YouTube accounts were banned. Facebook “fact-checks” everything we post. Spotify canceled us. Medium canceled us. Apple canceled us. Hvorfor? Because we believe in the truth prevailing, and that means we will continue to discuss “taboo” topics.

The 2020 presidential election was stolen. You can’t say that on Big Tech platforms without risking cancellation, but we’d rather get cancelled for telling the truth rather than staying around to repeat mainstream media’s lies. They have been covering it up since before the election and they’ve convinced the vast majority of conservative news outlets that they will be harmed if they continue to discuss voter fraud. We refuse to back down. The truth is the truth.

The lies associated with Covid-19 are only slightly more prevalent than the suppression of valid scientific information that runs counter to the prescribed narrative. We should be allowed to ask questions about the vaccines, for example, as there is ample evidence for concern. One does not have to be an “anti-vaxxer” in order to want answers about vaccines that are still considered experimental and that have a track record in a short period of time of having side-effects, including death. One of our stories about the Johnson & Johnson “vaccine” causing blood clots was “fact-checked” and removed one day before the government hit the brakes on it. These questions and news items are not allowed on Big Tech which is just another reason we are getting canceled.

There are more topics that they refuse to allow. In turn, we refuse to stop discussing them. This is why we desperately need your help. The best way NOQ, CP, and ACM readers can help is to donate. Vores Giving Fuel page makes it easy to donate one-time or monthly. Alternativt kan du donate through PayPal såvel. We are on track to be short by about $4100 per month in order to maintain operations.

The second way to help is to become a partner. We’ve strongly considered seeking angel investors in the past but because we were paying the bills, it didn’t seem necessary. Now, we’re struggling to pay the bills. We had 5,657,724 sessions on our website from November, 2020, through February, 2021. Our intention is to elevate that to higher levels this year by focusing on a strategy that relies on free speech rather than being beholden to progressive Big Tech companies.

During that four-month stretch, Twitter and Facebook accounted for about 20% of our traffic. We are actively working on operating as if that traffic is zero, replacing it with platforms that operate more freely such as Gab, Parler, and others. While we were never as dependent on Big Tech as most conservative sites, we’d like to be completely free from them. That doesn’t mean we will block them, but we refuse to be beholden to companies that absolutely despise us simply because of our political ideology.

We’re heading in the right direction and we believe we’re ready talk to patriotic investors who want to not only “get in on the action” but more importantly who want to help America hear the truth. Interested investors should contact me directly with the contact button above.

As the world spirals towards radical progressivism, the need for truthful journalism has never been greater. But in these times, we need as many conservative media voices as possible. Please help keep NOQ Report going.


Se videoen: Virus (August 2022).