Alpha/beta interferons increase host resistance to murine AIDS

Area of Science:

• Immunology
• Virology
• Retroviral Infections

Background:

• Murine AIDS (MAIDS) is induced by the LP-BM5 retrovirus mixture.
• Mouse strains exhibit varying susceptibility to MAIDS, with C57BL/6 being susceptible and CBA/B10.BR being resistant.
• Previous studies indicated an early block in viral replication in resistant mice.

Purpose of the Study:

• To investigate the potential role of alpha/beta interferons (IFN-alpha/beta) in host resistance to MAIDS.
• To determine if IFN-alpha/beta production correlates with resistance or susceptibility to LP-BM5 infection.

Main Methods:

• Infection of susceptible C57BL/6 mice with LP-BM5 retrovirus.
• Treatment of infected mice with exogenous IFN-alpha/beta or Newcastle disease virus (NDV) to induce endogenous IFN production.
• Assessment of MAIDS development through splenomegaly and T-/B-cell proliferation.
• Detection of IFN-alpha/beta response using reverse transcription-PCR and dot blotting at various time points post-infection.

Main Results:

• Treatment with IFN-alpha/beta or NDV delayed MAIDS progression in susceptible mice.
• Resistant mice demonstrated an early IFN-alpha/beta response to LP-BM5 infection (3-9 hours post-infection).
• Susceptible mice did not exhibit an early IFN-alpha/beta response after LP-BM5 infection.

Conclusions:

• The capacity to produce alpha/beta interferons (IFN-alpha/beta) early after retroviral infection contributes to host resistance against Murine AIDS (MAIDS).
• IFN-alpha/beta may be a critical factor in the innate immune response controlling LP-BM5 replication and MAIDS pathogenesis.