Implications of Sin Nombre Virus on Immune System Function and the Rate of Co-infection with Bartonella on Peromyscus maniculatus

Our research is focused on Sin Nombre virus (SNV) which is endemic to the southwestern US and causes severe illness and death in humans. The primary host of SNV is the deer mouse (Peromyscus maniculatus), a species that retains life-long infection showing few outward symptoms. We hypothesized that chronic SNV infection could result in a reduction in the immunocompetence of deer mice.  Reductions in immunocompetence could have implications for human health, as immuncompromised deer mice are more likely to shed intact SNV in their urine, saliva and feces, resulting in possible human infection.  To determine whether SNV infection reduces immunocompetence, adult deer mice were live trapped and screened for infection.  We then compared immune capacity of SNV-infected and SNV-uninfected mice. We used ELISA to measure circulating levels of C-reactive protein, a marker of inflammatory immune response. Secondly, we assessed innate immunity by culturing deer mouse serum with E. coli, quantifying antibacterial killing capacity. Lastly, we used PCR to screen deer mice for co-infection with Bartonella, a bacterial pathogen that is endemic in North American rodents. Co-infection with Bartonella was used as a proxy to determine whether deer mice infected with SNV are more susceptible to infection with other pathogens. Our preliminary results indicate that SNV-infected deer mice have reductions in immunocompetence, significantly reduced antibacterial killing capacity and greater rates of Bartonella co-infection compared to SNV-uninfected deer mice. SNV-infected deer mice had elevated CRP levels compared to their uninfected counterparts, confirming that SNV infection requires a constant, low level, immune response.