Rare co-existence of rodent-borne arenavirus patterns and autoimmune-like systemic flares: novel microbiome markers for public health risk stratification

To the Editor, Emerging evidence suggests that rodent-borne arenaviruses, particularly lymphocytic choriomeningitis virus (LCMV), are capable of inducing immune dysregulation that may clinically resemble autoimmune disease. Viral infections have long been implicated in triggering the breakdown of immune tolerance through mechanisms, such as molecular mimicry, bystander activation, and chronic immune stimulation, complicating differentiation between infectious and autoimmune etiologies in clinical practice[1]. Arenavirus–host interactions demonstrate complex immune modulation, particularly involving T-cell-mediated responses that may lead to immunopathology rather than direct cytotoxic injury. Experimental models of LCMV infection have shown that persistent viral antigen exposure can alter immune responses and drive chronic immune activation, highlighting a well-established mechanism of infection-associated immune dysregulation and tissue injury[2]. Furthermore, viral infections are recognized contributors to autoimmunity through multiple immune pathways, including dysregulated inflammatory signaling and sustained immune activation. Evidence indicates that viral triggers can precipitate autoimmune disease through mechanisms involving aberrant immune activation and loss of self-tolerance, supporting the biological plausibility of autoimmune-like clinical presentations following infection[3]. Recent advances in microbiome research indicate that gut microbial composition plays a central role in regulating antiviral immunity and systemic inflammatory tone. Dysbiosis has been associated with altered immune homeostasis and impaired antiviral responses, suggesting that microbiome signatures may serve as early non-invasive biomarkers of immune perturbation during infectious disease states[4]. Importantly, microbiota–immune system interactions have been shown to regulate systemic antiviral immunity, including type I interferon responses and inflammatory severity during infection. This supports the hypothesis that gut microbiome profiling may offer a non-invasive strategy for early risk stratification in zoonotic viral exposure settings[5]. Integrated surveillance frameworks combining virological monitoring, serological screening, and microbiome-based profiling may, therefore, improve early detection of immune dysregulation in rodent-endemic regions. Such hybrid systems could enhance public health preparedness by identifying individuals at risk of developing autoimmune-like systemic inflammatory responses following zoonotic exposure.