Molecular mimicry, viruses proteins

Various viruses encode proteins with sequenee homology to host proteins which are known to be involved in host defense functions. Viruses pirate and modify key immunoregulatory molecules, by use of molecular mimicry, to elude the Immune system (Murphy, 1997). Viruses also encode proteins that exploit or alter their host cells, replicate or induce migration for virus dissemination. Interestingly, DNA viruses such as the Herpesviruses (Cytomegalovirus (CMV), human herpesvirus (HHV-6 and 7), herpesvirus Saimiri (HVS) and Kaposi s sarcoma-associated Herpesvirus (KSHV)) all express GPCRs (Table 2). 

TlDM was previously known as insulin-dependent diabetes meUi-tus (IDDM) and juvenile-onset diabetes (JOD). It occurs in 0.5% of the population, and is characterised by sudden onset, usually before 25 years of age, and weight loss. The -cells are destroyed by autoimmune attack following viral infection. Molecular mimicry is thought to be the cause. This happens when parts of a virus protein resembie a protein in the host s P-cells. The body s immune defences then attack both the virus and the P-cells, which are destroyed hence insulin secretion ceases causing TIDM. 

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