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Effect of immunodeficiency on MPV shedding and transmission
James D Macy1, Frank X Paturzo, Susan R Compton
1Section of Comparative Medicine, School of Medicine, Yale University, New Haven, CT, USA. james.macy@yale.edu
Abstract:
C57BL/6 (B6) mice briefly shed low levels of MPV, and transmission is inefficient. To determine whether deficits in B or T cells or in interferon γ on a B6 background increased the duration of MPV shedding or transmission, B-cell-deficient (Igh), interferon-γ-deficient (Ifnγ), B- and T-cell-deficient (Rag), and B6 mice were inoculated with MPV. At 1 and 2 wk postinoculation (wpi), 11% to 94% of mice shed MPV. From 4 to 18 wpi, 80% to 100% of Rag mice and 0% of B6 and Ifnγ mice shed MPV; Igh mice sporadically shed MPV through 20 wpi. MPV was transmitted from B6 mice and Ifnγ mice at 2 to 4 wpi. Rag and Igh mice transmitted MPV to sentinels at all or most time points, respectively, between 2 to 16 wpi. Once transmission ceased from B6, Ifnγ, and Igh mice, breeding trios were setup and showed that MPV was transmitted to offspring in only one cage of Igh mice. In another experiment, MPV shedding ceased from B6, CD8-deficient (CD8), CD4-deficient (CD4), and T-cell-receptor-deficient (TCR) mice by 2, 6, 8, and 8 wpi, respectively. MPV was transmitted to sentinels only at 1 to 4 wpi. Mesenteric lymph nodes collected from 61% to 100% of B6, Ifnγ, TCR, CD4, CD8, and Rag mice were MPV DNA-positive. In conclusion, MPV transmission did not differ between mice deficient in T cell functions or Ifnγ and B6 mice. In contrast, B-cell deficiency posed an increased risk for MPV transmission in mice.
Insights
Murine polyomavirus (MPV) shedding and transmission were studied in mice with immune deficiencies. B-cell deficiency significantly increased MPV transmission risk, while T-cell or interferon-gamma deficiencies did not alter transmission compared to wild-type mice.
Area of Science:
- Immunology
- Virology
- Mouse Models
Background:
- Murine polyomavirus (MPV) is typically shed briefly at low levels in C57BL/6 (B6) mice, with inefficient transmission.
- The role of specific immune components, such as B cells, T cells, and interferon-gamma (Ifnγ), in MPV shedding and transmission duration is not fully understood.
Purpose of the Study:
- To investigate how deficiencies in B cells, T cells, or interferon-gamma affect the duration of MPV shedding and transmission in a mouse model.
- To determine the impact of specific immune cell deficits on MPV transmission dynamics.
Main Methods:
- MPV inoculation in B-cell-deficient (Igh), interferon-γ-deficient (Ifnγ), B- and T-cell-deficient (Rag), and wild-type B6 mice.
- Monitoring of MPV shedding and transmission to sentinel mice at various time points post-inoculation (wpi).
- Analysis of MPV DNA in mesenteric lymph nodes and transmission to offspring via breeding trios.
Main Results:
- Rag mice exhibited prolonged MPV shedding (up to 18 wpi), while B6 and Ifnγ mice shed MPV briefly. Igh mice showed sporadic shedding through 20 wpi.
- MPV transmission occurred from B6 and Ifnγ mice between 2-4 wpi. Rag and Igh mice transmitted MPV more persistently (up to 16 wpi).
- B-cell deficiency (Igh) significantly increased MPV transmission risk to offspring and sentinels compared to B6, Ifnγ, and T-cell deficient (CD4, CD8, TCR) mice.
Conclusions:
- Deficiencies in T-cell functions or interferon-gamma did not significantly alter MPV transmission compared to wild-type B6 mice.
- B-cell deficiency is identified as a key factor increasing the risk and duration of MPV transmission in mice.
- The study highlights the critical role of B cells in controlling MPV shedding and preventing sustained transmission.
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