Abstract
Parasites, bacteria, and viruses pose serious threats to public health. Many parasite infections, including infections of protozoa and helminths, can inhibit inflammatory responses and impact disease outcomes caused by viral, bacterial, or other parasitic infections. Type I interferon (IFN-I) has been recognized as an essential immune effector in the host defense against various pathogens. In addition, IFN-I responses induced by co-infections with different pathogens may vary according to the host genetic background, immune status, and pathogen burden. However, there is only limited information on the roles of IFN-I in co-infections with parasites and viruses, bacteria, or other parasites. This review summarizes some recent findings on the roles of IFN-I in co-infections with parasites, including Leishmania spp., Plasmodium spp., Eimeria maxima, Heligmosomoides polygyrus, Brugia malayi, or Schistosoma mansoni, and viruses or bacteria and co-infections with different parasites (such as co-infection with Neospora caninum and Toxoplasma gondii, and co-infection with Plasmodium spp. and H. polygyrus). The potential mechanisms of host responses associated with co-infections, which may provide targets for immune intervention and therapies of the co-infections, are also discussed.
Highlights
Interferons (IFNs) were initially discovered as soluble effector molecules influencing viral replication in 1957 [1]
Mice co-infected with the gastrointestinal helminths Trichinella spiralis or H. polygyrus and mouse norovirus showed increased viral loads and reduced levels of virus-specific CD4+ T cells expressing IFNγ and tumor necrosis factor α (TNFα) than mice infected with norovirus alone, indicating helminth infection suppresses antiviral immunity [24]
The innate IFNα response induced via toll-like receptor 7 (TLR7)/9 by human immunodeficiency virus (HIV)-1 or HSV1 in human plasmacytoid dendritic cell (pDC) is suppressed by rhoptry protein 16 (ROP16) kinase of T. gondii through IL-10 mediated inhibition of herpes simplex virus (HSV)-induced IRF7 nuclear translocation [23]
Summary
Interferons (IFNs) were initially discovered as soluble effector molecules influencing viral replication in 1957 [1]. IFNα, IFNβ, TNFα, and IL-6 genes were induced, and splenic T cells and DCs were activated in ECM, which were reversed in IFNAR1−/− mice [18]. Mice co-infected with the gastrointestinal helminths Trichinella spiralis or H. polygyrus and mouse norovirus showed increased viral loads and reduced levels of virus-specific CD4+ T cells expressing IFNγ and TNFα than mice infected with norovirus alone, indicating helminth infection suppresses antiviral immunity [24].
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