Worldwide more than 2 billion people are infected with helminths, predominantly in developing countries.
Co-infections with viruses such as human immunodeficiency virus (HIV) are common due to the geographical overlap of these pathogens. Helminth and
viral infections induce antagonistic
cytokine responses in their hosts. Helminths shift the immune system to a type 2-dominated immune response, while
viral infections skew the
cytokine response towards a type 1 immune response. Moreover, chronic helminth
infections are often associated with a generalized suppression of the immune system leading to prolonged parasite survival, and also to a reduced defence against unrelated pathogens. To test whether helminths affect the outcome of a
viral infection we set up a filarial/retrovirus
co-infection model in C57BL/6 mice. Although Friend virus (FV)
infection altered the L. sigmodontis-specific
immunoglobulin response towards a type I associated
IgG2 isotype in co-infected mice, control of L. sigmodontis
infection was not affected by a FV-
superinfection. However, reciprocal control of FV
infection was clearly impaired by concurrent L. sigmodontis
infection. Spleen weight as an
indicator of pathology and viral loads in spleen, lymph nodes (LN) and bone marrow (BM) were increased in L. sigmodontis/FV-co-infected mice compared to only FV-infected mice. Numbers of FV-specific CD8+ T cells as well as
cytokine production by CD4+ and CD8+ cells were alike in co-infected and FV-infected mice. Increased viral loads in co-infected mice were associated with reduced titres of neutralising FV-specific
IgG2b and IgG2c
antibodies. In summary our findings suggest that helminth
infection interfered with the control of retroviral
infection by dampening the virus-specific neutralising antibody response.