Immune evasion strategies of viruses


Viruses are considered as extremely successful predators as they can replicate and control the host cell synthesizing machinery. Viruses have coevolved with their hosts and thus have limited pathogenicity in any immunocompromised natural host. Viruses can exist in two forms: extra cellular virion particles and intracellular genomes. Virions are more resistant to physical stress than genomes but are susceptible to humoral immune control. Nevertheless, to exist as a species, virus replication and transfer to a new host are essential. These processes are associated with the production of antigenic proteins that make the virus vulnerable to immune control mechanisms ‘warning’ the host of the presence of an invader . There are two classes of viral immunoregulatory proteins: the proteins encoded by genes having sequence similarity with cellular genes and those coded by genes without any sequence similarity to cellular genes. The second class of protein may represent a paradigm for co-evolution.

Infection with the human and simian immunodeficiency viruses are unique in that the infections give rise to prolonged, continuous viral replication in the infected host. Destruction of virus-specific T helper cells, the emergence of antigenic escape variants and the expression of an envelope complex that structurally minimizes antibody escape to conserved epitopes contribute to persistence. Moreover, the virus encoded protein Nef prevents the viral antigen presentation.

CSF virus (CSFV) has high affinity for vascular endothelial cells and lymphoreticular cells including T cells, B cells and monocytes. Severe depletion of B cells and T cells in Peripheral Blood Mononuclear Cells (PBMC) and virus persistence in lymphoid tissues is thought to be the most important characteristics of CSFV infection that leads to the acquired immunosuppressive state.

Blocking B-lymphocyte maturation by infection and destruction of germinal centers is a key event in the pathogenesis of acute, lethal CSF before the development of generalized infection. Immature B lymphocytes can themselves be the cellular targets of the virus in any stage of maturation within follicles or they may lack critical cytokines because of an infection of the supporting follicular dendritic cell network. However, it is clear that depletion of B lymphocytes cannot account for all the pleiotropic symptoms of this disease. But, as it is generally held that antibodies against CSF can be protective and as recovery from acute infection is known to be associated with seroconversion. It appears justified that B-follicle tropism of an HCV isolate is an important determinant for the course of disease.

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Sophie Kate
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Microbiology: Current Research