Does SARS-CoV-2 Trigger Stress-InducedAutoimmunity by Molecular Mimicry? A Hypothesis

Area of Science:

• Virology
• Immunology
• Pathogenesis

Background:

• Viruses are known to induce molecular mimicry, where viral components resemble host molecules.
• This phenomenon can lead to the immune system mistakenly attacking the host's own tissues.
• The potential for SARS-CoV-2 to engage in molecular mimicry remains largely unexplored.

Purpose of the Study:

• To explore the hypothesis that SARS-CoV-2 can induce molecular mimicry.
• To investigate the possibility of SARS-CoV-2-induced antibodies cross-reacting with host antigens.
• To understand the potential autoimmune consequences of SARS-CoV-2 infection.

Main Methods:

• This review synthesizes existing knowledge on viral molecular mimicry.
• It proposes a working hypothesis for SARS-CoV-2-mediated autoimmunity.
• Suggests the need for in vitro and in vivo experimental validation.

Main Results:

• The review posits that SARS-CoV-2 may induce antibodies that cross-react with host antigens.
• This cross-reactivity could initiate autoimmune phenomena.
• Such autoimmune responses may have severe consequences across various host tissues and organs.

Conclusions:

• SARS-CoV-2 could be a potential trigger for autoimmune diseases via molecular mimicry.
• Confirmation of this hypothesis requires rigorous experimental testing.
• If validated, this understanding could pave the way for novel therapeutic strategies against SARS-CoV-2.