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Interactions between murine AIDS (MAIDS) and toxoplasmosis in co-infected mice
C Lacroix1, M Levacher-Clergeot, F Chau
1Institut National de la Santé et de la Recherche Médicale, Unité 13, Paris, France.
Abstract:
We coinfected C57B1/6 mice with LP-BM5 murine leukaemia viruses, responsible for murine AIDS (MAIDS), and an avirulent strain of Toxoplasma gondii. Virus-infected mice were infected perorally on day 30 with 10 cysts of T. gondii, and T. gondii-infected mice were challenged with LP-BM5 on day 20, 30 or 60 after parasite inoculation. Uninfected and singly infected mice were used as controls. The kinetics of parasite burden in blood, lungs and brain, together with blood lymphocyte subsets, and spleen and lymph node weights, were serially determined in each group of mice. The kinetics of parasite counts in mice infected by LP-BM5 then by T. gondii were similar to those in mice infected by T. gondii only, except for lung counts, which reached higher values than in animals infected with T. gondii alone, then fell and re-increased until the end of the experiment. The only significant change in parasite burdens when mice were first infected by T. gondii and then by LP-BM5, compared with T. gondii controls, was an increase in lung counts in mice challenged with LP-BM5 20 days after T. gondii inoculation. Whatever the schedule of co-infection, the kinetics of lymphocyte subsets in co-infected mice differed from those in T. gondii- or LP-BM5-infected mice; in dually infected mice CD4+ and CD8+ cell counts were intermediate between values in mice singly infected by the parasite or the virus. Enlargement of spleen and lymph nodes, which is a major criterion of MAIDS progression, was significantly less marked in co-infected mice than in mice infected with LP-BM5 alone. These data point to cross-regulation of T. gondii and LP-BM5 infections, which results in increased susceptibility to T. gondii, and may alter the progression of MAIDS.
Insights
Coinfection with Toxoplasma gondii and LP-BM5 murine leukemia virus alters immune responses. Dual infection increases susceptibility to T. gondii and may impact murine AIDS progression.
Area of Science:
- Immunology
- Infectious Diseases
- Virology
Background:
- Murine AIDS (MAIDS) is caused by LP-BM5 murine leukemia viruses.
- Toxoplasma gondii is an opportunistic parasite.
- Understanding coinfection dynamics is crucial for immune response modulation.
Purpose of the Study:
- To investigate the effects of coinfecting C57B1/6 mice with LP-BM5 virus and T. gondii.
- To analyze the impact of infection order and timing on parasite burden and immune cell populations.
- To determine how coinfection influences MAIDS progression.
Main Methods:
- Mice were coinfected with LP-BM5 virus and T. gondii using different schedules.
- Parasite burden in blood, lungs, and brain was monitored.
- Lymphocyte subsets (CD4+, CD8+), spleen, and lymph node weights were analyzed.
- Control groups included singly infected and uninfected mice.
Main Results:
- Coinfection altered parasite kinetics, notably increasing lung parasite burden.
- Dual infection led to intermediate CD4+ and CD8+ T-cell counts compared to single infections.
- Enlargement of spleen and lymph nodes, a MAIDS indicator, was less pronounced in coinfected mice.
- The timing of T. gondii challenge after LP-BM5 infection influenced lung parasite levels.
Conclusions:
- T. gondii and LP-BM5 infections exhibit cross-regulation.
- Coinfection may increase susceptibility to T. gondii.
- Dual infection appears to modulate MAIDS progression, potentially mitigating some symptoms.