Virus-induced immunopathology

The immune response mounted against an invading virus may itself be responsible for the damage and disease state that follow infection. This  is the  case  for the  majority of the  common cold  symptoms seen with  rhinovirus infections and  the  skin  rash  that is associated with  measles. We have described symptomatic and asymptomatic chronic HBV infections; the major contributor to the symptomatic outcome is immune lysis of infected hepatocytes by CTLs. The recently emerged SARS virus itself causes little cellular damage, but it stimulates a ‘cytokine storm’ in patients, a heightened release of immune proteins that lead to an inappropriate and dangerous immune response. Dengue virus has four known serotypes and infection with any single serotype gives rise to a febrile illness with an accompanying rash and joint and muscle pain. However, subsequent infection with a different strain of Dengue virus, especially in children, leads to a much more severe pathology, dengue hemorrhagic shock syndrome (DHSS), thought to be  due  to the enhanced immune response to the second strain. Viruses may also evoke autoimmu- nity, probably via molecular mimicry, which is the production of an antigen that shares conserved sequences with a host cell protein. As a result, antibodies or T cells are produced with specificity against the viral antigen but that also react with host proteins.