HIV and HCV Activate the Inflammasome in Monocytes and Macrophages via Endosomal Toll-Like Receptors without Induction of Type 1 Interferon


Pathogens are detected by the immune system in multiple ways that initiate responses to control infection. Two systems of first line defense against viruses are 1) the production of Type I interferons and 2) production of the cytokines IL-1β and IL-18 by the inflammasome. Type I interferons promote an antiviral state in the infected host. Inflammasome cytokines induce inflammation, modulate adaptive immune responses, and have direct antiviral effects. While both are produced in response to the chronic human viral infections HIV and HCV, we demonstrate here that inflammasome activation does not require cell infection and that the mechanisms for viral sensing as well as cell types in which sensing occurs are distinct between the two viruses and between the type I interferon vs. inflammasome systems. The relative amount of sensing via these different mechanisms may affect the balance between antiviral and inflammatory responses to chronic infection.


Vyšlo v časopise: HIV and HCV Activate the Inflammasome in Monocytes and Macrophages via Endosomal Toll-Like Receptors without Induction of Type 1 Interferon. PLoS Pathog 10(5): e32767. doi:10.1371/journal.ppat.1004082
Kategorie: Research Article
prolekare.web.journal.doi_sk: 10.1371/journal.ppat.1004082

Souhrn

Pathogens are detected by the immune system in multiple ways that initiate responses to control infection. Two systems of first line defense against viruses are 1) the production of Type I interferons and 2) production of the cytokines IL-1β and IL-18 by the inflammasome. Type I interferons promote an antiviral state in the infected host. Inflammasome cytokines induce inflammation, modulate adaptive immune responses, and have direct antiviral effects. While both are produced in response to the chronic human viral infections HIV and HCV, we demonstrate here that inflammasome activation does not require cell infection and that the mechanisms for viral sensing as well as cell types in which sensing occurs are distinct between the two viruses and between the type I interferon vs. inflammasome systems. The relative amount of sensing via these different mechanisms may affect the balance between antiviral and inflammatory responses to chronic infection.


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Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

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