It is known that infections with certain viruses can weaken the immune response to another pathogen. A study published online on May 21, 2015 in the open-access journal PLOS Pathogens reports provocative findings in mice indicating that infection with the mouse equivalent of Epstein-Barr virus (EBV)(image) can turn infections with certain parasites that cause malaria in mice (infections that are normally quickly suppressed by the mouse immune system) into a lethal disease. The article is titled “Gammaherpesvirus Co-infection with Malaria Suppresses Anti-Parasitic Humoral Immunity.” In Sub-Saharan Africa, infants are infected with EBV, a gamma-herpesvirus that infects B cells and, like HIV, remains present throughout the lifetime of the host. Children infected with EBV who live in areas where malaria is common have an increased risk of developing Burkitt's lymphoma, a cancer linked to EBV. To investigate whether EBV infection could also affect the course of malaria disease, a team of researchers led by Dr. Tracey Lamb and Dr. Samuel Speck, both from Emory University, Atlanta, Georgia, USA, studied the consequences of co-infection with of a gamma-herpesevirus and two different parasites that cause malaria in mice. Where normally immune cells expand and mount a rapid and precise defense against an intruder, acute murine gamma-herpesvirus 68 (MHV68) infections of mice, like acute EBV infections in humans, can induce a transient suppression of the antibody immune response during a subsequent infection by another pathogen. The researchers used two well-established, non-lethal strains of mouse parasites called Plasmodium yoelii XNL and Plasmodium chabaudi AS, and determined that acute MHV68 infection can suppress the anti-malarial antibody response during co-infection with either of these Plasmodium strains.
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