Immune Regulation and Evasion of Mammalian Host Cell Immunity During Viral Infection

Abstract

The mammalian host immune system has wide array of defence mechanisms against viral infections. Depending on host immunity and the extent of viral persistence, either the host immune cells might clear/restrict the viral load and disease progression or the virus might evade host immunity by down regulating host immune effector response(s). Viral antigen processing and presentation in the host cells through major histocompatibility complex (MHC) elicit subsequent anti-viral effector T cell response(s). However, modulation of such response(s) might generate one of the important viral immune evasion strategies. Viral peptides are mostly generated by proteolytic cleavage in the cytosol of the infected host cells. CD8 ? T lymphocytes play critical role in the detection of viral infection by recognizing these peptides displayed at the plasma membrane by MHC-I molecules. The present review summarises the current knowledge on the regulation of mammalian host innate and adaptive immune components, which are operative in defence mechanisms against viral infections and the variety of strategies that viruses have evolved to escape host cell immunity. The understanding of viral immune evasion strategies is important for designing anti-viral immunotherapies.

Regulation of Viral Replication, Apoptosis and Pro-Inflammatory Responses by 17-AAG during Chikungunya Virus Infection in Macrophages

“…Viral infection in APCs like macrophages is known to enhance antigen processing and presentation via MHC to elicit adaptive immune responses. However, some viruses are known to manipulate the expression of MHC and co-stimulatory molecules to evade host cell immunity [ 32 , 68 , 69 , 70 , 71 ]. Moreover, our recent in silico analysis has identified several highly conserved CHIKV specific immunodominant MHC-I restricted peptide epitopes which may elicit strong anti-CHIKV CD8 + T cell responses [ 88 ].…”

“…CHIKV targets a wide range of immune and non-immune cells for its replication, propagation and dissemination. Among them, antigen presenting cells (APCs) such as macrophages/monocytes are known to play important roles towards modulating adaptive immune response against pathogens [ 31 , 32 , 33 , 34 , 35 ]. Among blood leukocytes, monocytes are known to be the major host cells for acute CHIKV infection in humans [ 36 ].…”

DA virus mutant H101 has altered CNS pathogenesis and causes immunosuppression

“…As viruses develop new ways to evade the host immune response, the host, if it is to survive, must develop new ways to combat the viral infection. There are a multitude of viral immune evasion strategies that function through down regulation of both innate and adaptive components of the host immune response (Pratheek, et al 2013). Some mechanisms of evasion lead to defective viral antigen processing and presentation and therefore no effector T cell response is induced.…”

“…Some mechanisms of evasion lead to alteration in the host cellular microenvironment (cytokines and chemokines), thus altering the effector T cell response possibly through the induction of a regulatory T cell response. Yet other mechanisms of evasion involve the targeting of different immune cell types, such as natural killer cells, B cells or dendritic cells, or the regulation of the host complement system, which is a mechanism known to be used by picornavirus (Pratheek, et al 2013). The H101 mutant strain of TMEV has acquired a new mechanism of evasion: the ability to target T cells that are critical to the host’s ability to combat the viral infection and clear the virus.…”

Host–virus interaction and viral evasion

“…Host cells are protected against the action of the complement system by the expression of complement activation regulators (RCA) in their membranes. These RCAs negatively regulate complement activity, inhibiting the formation of C3 (C3 convertase) activation enzymes and preventing the formation of the membrane attack complex (Pratheek et al, 2013; Ricklin, 2012).…”