Gammaherpesvirus Co-infection with Malaria Suppresses Anti-parasitic Humoral Immunity
Nearly 1 million deaths occur annually as a result of complications associated with P. falciparum infection, with children younger than 5 being the most susceptible age group. Earlier studies have demonstrated that children co-infected with P. falciparum and Epstein-Barr virus (EBV) have impaired immune responses to control EBV, and this can result in the development of a jaw tumor called endemic Burkitt’s lymphoma (eBL). It is not known if there is any impact of acute EBV infection on the generation of anti-malarial immunity. We have used mouse models of EBV [murine gammaherpesvirus 68 (MHV68)] and malaria (P. yoelii XNL) to demonstrate that acute gammaherpesvirus infection can impair the generation of antibodies that control Plasmodium parasitemia, in turn causing a non-lethal P. yoelii XNL infection to become lethal. We identify a critical role for the MHV68 M2 protein in mediating the suppressive effect of acute MHV68 infection on the generation of humoral immunity to a secondary malaria infection. This work demonstrates that gammaherpesvirus infections can suppress the generation of an effective anti-malaria immune response and suggests that acute EBV infection should be investigated as a risk factor for the development of severe malaria in young children.
Vyšlo v časopise:
Gammaherpesvirus Co-infection with Malaria Suppresses Anti-parasitic Humoral Immunity. PLoS Pathog 11(5): e32767. doi:10.1371/journal.ppat.1004858
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1004858
Souhrn
Nearly 1 million deaths occur annually as a result of complications associated with P. falciparum infection, with children younger than 5 being the most susceptible age group. Earlier studies have demonstrated that children co-infected with P. falciparum and Epstein-Barr virus (EBV) have impaired immune responses to control EBV, and this can result in the development of a jaw tumor called endemic Burkitt’s lymphoma (eBL). It is not known if there is any impact of acute EBV infection on the generation of anti-malarial immunity. We have used mouse models of EBV [murine gammaherpesvirus 68 (MHV68)] and malaria (P. yoelii XNL) to demonstrate that acute gammaherpesvirus infection can impair the generation of antibodies that control Plasmodium parasitemia, in turn causing a non-lethal P. yoelii XNL infection to become lethal. We identify a critical role for the MHV68 M2 protein in mediating the suppressive effect of acute MHV68 infection on the generation of humoral immunity to a secondary malaria infection. This work demonstrates that gammaherpesvirus infections can suppress the generation of an effective anti-malaria immune response and suggests that acute EBV infection should be investigated as a risk factor for the development of severe malaria in young children.
Zdroje
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Hygiena a epidemiológia Infekčné lekárstvo LaboratóriumČlánok vyšiel v časopise
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