Identification of Friend murine retrovirus-infected immune cells and studies of the effects of sex and steroid hormones in the early phase of infection
| Autor: | Liss Anne S. Lavik, Torunn Bruland, Hong Yan Dai, Are Dalen |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Male
Microbiology (medical) medicine.medical_specialty CD8-Positive T-Lymphocytes Dexamethasone Virus Pathology and Forensic Medicine Mice Sex Factors Immune system Retrovirus Internal medicine medicine Animals Immunology and Allergy Viremia Glucocorticoids Progesterone Hormone response element biology 3T3 Cells General Medicine Flow Cytometry biology.organism_classification Friend murine leukemia virus Endocrinology Viral replication Immunology biology.protein Female Antibody Orchiectomy Cell Division Spleen CD8 Retroviridae Infections Thymidine Hormone |
| Zdroj: | APMIS. 111:878-890 |
| ISSN: | 1600-0463 0903-4641 |
| Popis: | Male mice are more susceptible than female mice to the murine retrovirus FIS-2. We previously reported that sex-related factors influence early virus replication via mechanisms involving a glucocorticoid response element (GRE) in the long terminal repeat (LTR) enhancer region. In the present study, we investigated further the influence of sex and steroid hormones on early murine retrovirus dissemination and immune functions. In male mice we found a correlation between an early expansion of the CD8+ cell subset and rapid infection of lymphocytes, including CD8+ cells. Virus load in blood declined faster in females than in males, and the postpeak declines coincided with more rapidly generation of antibodies against virus-positive cells. Moreover, female-derived T-cells responded better to in vitro mitogen stimuli than male-derived T-cells. Physiological concentrations of progesterone and dexamethasone induced a dose-dependent inhibition of T-cell proliferation. Administration of progestin in vivo did not modify early FIS-2 production in female mice. Male castrated mice, who were notably less involved in aggressive behaviour and fighting compared to male control mice, had a significant delay of virus dissemination. We suggest that testosterone-dependent aggression, with successive enhanced stress hormone levels, may influence both FIS-2 replication and immune responses during infection. |
| Databáze: | OpenAIRE |
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