The mechanism of immune dysregulation caused by porcine reproductive and respiratory syndrome virus (PRRSV)

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F23%3A00578827" target="_blank" >RIV/67985904:_____/23:00578827 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/61388971:_____/23:00578827 RIV/00027162:_____/23:N0000131

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/pii/S1286457923000497?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S1286457923000497?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.micinf.2023.105146" target="_blank" >10.1016/j.micinf.2023.105146</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The mechanism of immune dysregulation caused by porcine reproductive and respiratory syndrome virus (PRRSV)

Popis výsledku v původním jazyce

PRRSV is capable of evading the effective immune response, thus persisting in piglets and throughout the swine herd. We show here that PRRSV invades the thymus and causes depletion of T-cell precursors and alteration of the TCR repertoire. Developing thymocytes are affected during negative selection when they transit from the triple-negative to triple-positive stages at the corticomedullary junction just before entering the medulla. The restriction of repertoire diversification occurs in both helper and cytotoxic abT cells. As a result, critical viral epitopes are tolerated, and infection becomes chronic. However, not all viral epitopes are tolerated. Infected piglets develop antibodies capable of recognizing PRRSV, but these are not virus neutralizing. Further analysis showed that the lack of an effective immune response against the critical viral structures results in the absence of a germinal center response, overactivation of T and B cells in the periphery, robust production of useless antibodies of all isotypes, and the inability to eliminate the virus. Overall, the results show how a respiratory virus that primarily infects and destroys myelomonocytic cells has evolved strategies to disrupt the immune system. These mechanisms may be a prototype for how other viruses can similarly modulate the host immune system.

Název v anglickém jazyce

The mechanism of immune dysregulation caused by porcine reproductive and respiratory syndrome virus (PRRSV)

Popis výsledku anglicky

PRRSV is capable of evading the effective immune response, thus persisting in piglets and throughout the swine herd. We show here that PRRSV invades the thymus and causes depletion of T-cell precursors and alteration of the TCR repertoire. Developing thymocytes are affected during negative selection when they transit from the triple-negative to triple-positive stages at the corticomedullary junction just before entering the medulla. The restriction of repertoire diversification occurs in both helper and cytotoxic abT cells. As a result, critical viral epitopes are tolerated, and infection becomes chronic. However, not all viral epitopes are tolerated. Infected piglets develop antibodies capable of recognizing PRRSV, but these are not virus neutralizing. Further analysis showed that the lack of an effective immune response against the critical viral structures results in the absence of a germinal center response, overactivation of T and B cells in the periphery, robust production of useless antibodies of all isotypes, and the inability to eliminate the virus. Overall, the results show how a respiratory virus that primarily infects and destroys myelomonocytic cells has evolved strategies to disrupt the immune system. These mechanisms may be a prototype for how other viruses can similarly modulate the host immune system.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

<a href="/cs/project/GA20-03282S" target="_blank" >GA20-03282S: Virus reprodukčního a respiračního syndromu prasat (PRRSV) pozměňuje vývoj thymocytů a repertoár T lymfocytů</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Microbes and Infection

ISSN

1286-4579

e-ISSN

1769-714X

Svazek periodika

25

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

13

Strana od-do

105146

Kód UT WoS článku

001083571800001

EID výsledku v databázi Scopus

2-s2.0-85170238533