Related Experiment Videos
Molecular mimicry between Fc receptors and viral antigens
1Department of Pathology, University of Texas Health Science Center, Medical School, Houston 77030, USA.
Abstract:
Molecular mimicry has been characterized as the presence of common epitopes, either linear or conformational, shared by host and microbial determinants. Such cross-reactivity may lead to an autoimmune disease. On the other hand molecular mimicry between certain viral proteins and host determinant may protect invading virus to be eliminated by immune system and may promote persistence. In this mini-review I discuss the molecular mimicry of S peplomer protein of mouse hepatitis virus, strain JHM (MHV-JHM) to the host Fc gamma receptor (Fc gamma R). MHV-JHM induces in rodents acute encephalomyelitis and surviving animals develop demyelinating disease with concomitant persistent infection. We have demonstrated that rabbit IgG, but not is F(ab')2 fragments, monoclonal rat and mouse IgG and the rat 2.4G2 anti-Fc gamma R mab immunoprecipitated natural and recombinant S peplomer protein of several strains of MHV. Furthermore, MHV-JHM infected cells formed rosettes with anti-sheep red blood cell (SRBC) - antibody coated SRBC. The 2.4G2 anti-Fc gamma R mab are able to neutralize several strains of MHV, presumably by binding to S peplomer protein. Therefore, the Fc binding site of S is present on the surface of MHV-infected cells. This molecular mimicry between S peplomer protein of MHV-JHM and Fc gamma R has been extended to other members of Coronaviridae, namely bovine coronavirus and transmissible gastroenteritis virus but not to infectious bronchitis virus. The molecular mimicry of viral antigens to Fc receptors has been described also for members of Herpesviridae, namely Herpes simplex, cytomegalovirus and Varicella zoster.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Molecular mimicry allows viruses like mouse hepatitis virus to evade the immune system by mimicking host Fc gamma receptors. This mimicry aids viral persistence and infection, impacting diseases like encephalomyelitis.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Molecular mimicry involves shared epitopes between host and microbial factors, potentially causing autoimmunity or promoting viral persistence.
- Mouse hepatitis virus strain JHM (MHV-JHM) causes encephalomyelitis and persistent infections in rodents.
- Viral molecular mimicry can protect viruses from immune elimination.
Purpose of the Study:
- To investigate molecular mimicry between the S peplomer protein of MHV-JHM and host Fc gamma receptors (Fc gamma R).
- To explore the implications of this mimicry for viral persistence and immune evasion.
Main Methods:
- Immunoprecipitation assays using antibodies against Fc gamma R and MHV S peplomer protein.
- Rosette formation assays with MHV-JHM infected cells and antibody-coated red blood cells.
- Viral neutralization assays using anti-Fc gamma R monoclonal antibodies.
Main Results:
- Rabbit IgG, but not F(ab')2 fragments, and anti-Fc gamma R monoclonal antibodies immunoprecipitated MHV S peplomer protein.
- MHV-JHM infected cells formed rosettes with antibody-coated red blood cells, indicating Fc binding.
- Anti-Fc gamma R antibodies neutralized MHV strains, suggesting binding to the S peplomer protein.
Conclusions:
- The S peplomer protein of MHV-JHM mimics host Fc gamma receptors, with the Fc binding site exposed on infected cells.
- This molecular mimicry extends to other Coronaviridae (bovine coronavirus, transmissible gastroenteritis virus) but not all (infectious bronchitis virus).
- Similar mimicry of Fc receptors is observed in Herpesviridae (Herpes simplex, cytomegalovirus, Varicella zoster).