Pathology and Pathogenesis of Virus Infections

Abstract

While the term immunopathology was originally used to describe an aberrant immune response to autoantigen resulting in pathology, more recent developments in our understanding of virus-induced immunopathology have revealed that this can be linked to both an aberrant immune response to the virus itself as well as unfavorable virus-induced changes to the immune response as a whole; for example, lymphopenia following certain types of infections as well as the specific loss of CD4 T cells in HIV infection. Perhaps the most common virus-induced pathology is T-cell-induced destruction of host tissues. T-cell mediated pathologies occur through both direct and indirect mechanisms including the targeted cytolysis of the infected cell by effector T cells, the induction of apoptosis in infected cells and generalized tissue damage due to bystander effects of T-cell activation. Difficulties in establishing an animal model of hantavirus pulmonary syndrome (HPS) had greatly hampered progress in understanding the factors involved in pathogenesis. Perhaps the most widely examined example of antibody dependent enhancement (ADE) can be found in dengue virus infections. The process by which viruses may induce or enhance autoimmunity is hypothesized to occur by a number of mechanisms. Recent clinical trials for several different vaccines, where vaccinated groups had elevated risk for infection and or disease than their naive cohorts, have highlighted the necessity for continued basic science research into the precise mechanisms of virus-induced immunopathology. One example of this can be found in the vastly different outcomes achieved with different strategies in respiratory syncytial virus (RSV) vaccination.