C1qa, a component of the complement system, plays a pivotal role in immune responses, especially in the anti-microbial pathway within tissues [1]. It has been investigated as an invariant biomarker for tissue macrophages [1]. C1qa is also involved in gene-gene interactions and may be associated with the age-at-onset in familial amyloid polyneuropathy patients [3]. Additionally, it is related to pathways like HALLMARK_COMPLEMENT, which is correlated and activated with C1qa, and is considered a stimulated risk gene for atherosclerosis [4].

In a C1qa KO mouse model, C1qa deficiency enhanced susceptibility to mouse hepatitis virus A59 systemic infection. C1qa KO mice showed severe histopathological changes such as hepatocellular necrosis and interstitial pneumonia, along with higher viral copy numbers in organs compared to wild-type mice. This enhanced susceptibility was also associated with dramatic elevations in spleen IFN-γ, MIP-1α, and MCP-1 in C1qa KO mice, suggesting that activation of the classical complement pathway may be important for protecting the host against MHV A59 infection [2].

In conclusion, C1qa is crucial in immune-related functions, especially in anti-microbial responses and as a potential biomarker. The C1qa KO mouse model has been instrumental in revealing its role in viral infection susceptibility, providing insights into the importance of the classical complement pathway in protecting against certain viral infections like MHV A59.