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Infection and immunoregulation of T lymphocytes by parainfluenza virus type 3
S Sieg1, C Muro-Cacho, S Robertson
1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106-4943.
Abstract:
Human parainfluenza virus type 3 (HPIV3) is a major cause of disease in newborns and infants. It also has a striking potential to reinfect individuals throughout their lives, suggesting that HPIV3 does not induce lifelong immunity; however, the operative mechanism for the failure to prevent reinfection is not known. We have assessed the potential of the virus to infect nontransformed human T lymphocytes and have found that T cells are readily infected by the virus. Productive infection requires activation of the T cells and results in a marked inhibition of proliferation. Furthermore, our results indicate that exposure to the virus, even without overt expression of viral proteins as detected by immunohistology, profoundly alters the functional capacity of the T cells. The capacity of the virus to regulate T-lymphocyte function may play an important role in the failure of the virus to induce lifelong immunity.
Insights
Human parainfluenza virus type 3 (HPIV3) readily infects T lymphocytes, inhibiting their proliferation. This viral interaction with T cells may explain why HPIV3 infections do not provide lifelong immunity.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Human parainfluenza virus type 3 (HPIV3) causes significant infant illness and recurrent infections, indicating a lack of lifelong immunity.
- The mechanisms underlying HPIV3's failure to induce durable immunity remain unclear.
Purpose of the Study:
- To investigate the susceptibility of human T lymphocytes to HPIV3 infection.
- To determine the impact of HPIV3 infection on T-cell function and proliferation.
Main Methods:
- Assessed HPIV3 infection potential in nontransformed human T lymphocytes.
- Analyzed T-cell activation requirements for productive HPIV3 infection.
- Evaluated the effects of HPIV3 exposure on T-cell proliferation and functional capacity.
Main Results:
- Human T lymphocytes are readily infected by HPIV3 upon activation.
- HPIV3 infection leads to significant inhibition of T-cell proliferation.
- HPIV3 exposure alters T-cell functional capacity, even without overt viral protein expression.
Conclusions:
- HPIV3 can productively infect and functionally impair human T lymphocytes.
- The virus's ability to modulate T-cell function may be a key factor in the incomplete immunity observed after HPIV3 infection.
- Understanding HPIV3-T-cell interactions is crucial for developing effective vaccines and treatments.