Host Immune Response to Influenza A Virus Infection

Abstract

Influenza A viruses (IAVs) are contagious pathogens responsible for severe respiratory infection in humans and animals worldwide. Upon detection of IAV infection, host immune system aims to defend against and clear the viral infection. Innate immune system is comprised of physical barriers (mucus and collectins), various phagocytic cells, group of cytokines, interferons (IFNs), and IFN-stimulated genes, which provide first line of defense against IAV infection. The adaptive immunity is mediated by B cells and T cells, characterized with antigen-specific memory cells, capturing and neutralizing the pathogen. The humoral immune response functions through hemagglutinin-specific circulating antibodies to neutralize IAV. In addition, antibodies can bind to the surface of infected cells and induce antibody-dependent cell-mediated cytotoxicity or complement activation. Although there are neutralizing antibodies against the virus, cellular immunity also plays a crucial role in the fight against IAVs. On the other hand, IAVs have developed multiple strategies to escape from host immune surveillance for successful replication. In this review, we discuss how immune system, especially innate immune system and critical molecules are involved in the antiviral defense against IAVs. In addition, we highlight how IAVs antagonize different immune responses to achieve a successful infection.

Improving immunological insights into the ferret model of human viral infectious disease

“…Influenza‐specific ASCs were also increased by 37 d.p.i, highlighting the role of B cells in the resolution of infection . These observations suggest changes in the maturation status of B cells after activation and mirror observations in humans and mice (as reviewed in). MHC‐II is upregulated in B cells to induce germinal centre formation (GC) through cognate interactions with T follicular helper cells (T FH ).…”

The Class IV human deacetylase, HDAC11, exhibits anti‐influenza A virus properties via its involvement in host innate antiviral response

“…However, there was no significant change in the expression of IFNαR1 and IFNβ1 (Figure a). On the basis of this observation, we next investigated the IAV‐induced phosphorylation of transcription factor, signal transducer and activator of transcription 1 (STAT1)—one of the main inducers of innate antiviral cascade, and subsequent expression of IFN‐stimulated genes (ISGs; Chen et al, ; Iwasaki & Pillai, ; Schneider, Chevillotte, & Rice, ) in HDAC11‐depleted cells. To analyse the STAT1 phosphorylation, A549 cells, transfected with the control siRNA or HDAC11 siRNA‐1, were infected with PR8 as above.…”

“…This indicated a slow or delayed induction of host anti‐IAV response in the absence of HDAC11. To investigate this further, we compared the expression of ISGs: IFN‐induced transmembrane (IFITM) protein 1, 2, and 3, IFN‐stimulated gene 15 (ISG15), viperin, cholesterol‐25‐hydroxylase (CH25H), tripartite motif protein 22 (TRIM22), myxovirus‐resistance protein‐1 (MX‐1), oligoadenylate synthetase 3 (OAS3), and the retinoic acid inducible gene‐1 (RIG‐I) effector mitochondrial antiviral signalling protein (MAVS) that have been implicated in virus infections including IAV (Chen et al, ; Iwasaki & Pillai, ; Schneider et al, ), in control and HDAC11‐depleted cells in response to PR8 infection by qPCR. Consistent with the above findings, there was a significant 44% ( P = 0.013), 44% ( P = 0.007), 42% ( P = 0.026), 45% ( P = 0.03), 38% ( P = 0.039), 39% ( P = 0.019), 45% ( P = 0.017), and 42% ( P = 0.016) reduction in the expression of IFITM1, IFITM2, IFITM3, ISG15, viperin, CH25H, TRIM22, and MX‐1 transcripts, respectively, in HDAC11‐depleted cells compared with the control cells (Figure d).…”

Проблема Бактериальных Осложнений При Респираторных Вирусных Инфекциях

“…Система врожденного противовирусного иммуни-тета подробно описана в обзорах [74,75]. Защитная функция IFN обусловлена двумя основными факто-рами: способностью индуцировать синтез множества противовирусных белков в зараженных и окружаю-щих их клетках и иммуномодулирующими функци-ями, влияющими на миграцию и активацию клеток врожденного иммунитета и определяющими разви-тие специфического В-и Т-клеточного иммунного ответа [76][77][78].…”