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DOI 10.1016/s1386-6532(99)00002-5

Медицинская библиотека · Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 1999

Measles virus infection causes transient depletion of activated T cells from peripheral circulation.

Nanan R, Chittka B, Hadam M, Kreth H W

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Аннотация

BACKGROUND

Natural measles virus infection as well as vaccination with attenuated measles virus induce temporary immunosuppression, which is responsible for part of the morbidity and mortality associated with measles. The underlying molecular mechanisms are not known. Recently, in vitro studies have revealed a marked increase of LFA-1 expression of lymphocytes in the presence of infectious measles virus.

OBJECTIVES

In order to further investigate immune dysfunction in measles we analyzed the expression of leukocyte function-associated antigen 1 (LFA-1) on ex vivo derived circulating human T cells.

STUDY

DESIGN

Expression of LFA-1 was measured by flow cytometry using monoclonal antibodies directed against CD11a and CD18. LFA-1 expression was followed in the course of infection in four adult seronegative vaccinees and in four patients with natural measles.

RESULTS

There was a remarkable loss of LFA-1-bright cells during natural measles and after measles vaccination. The number of LFA-1-bright cells reached a minimum on day 7-14 after vaccination, and at the onset of rash during natural measles infection, and approached normal levels within 3-5 weeks.

CONCLUSION

It is suggested that measles virus infection interferes with lymphocyte trafficking and reallocation. Disruption of recirculation and random homing of lymphocytes might contribute to the immunosuppression, which is characteristic for measles virus infection.

Для цитирования: Nanan R, Chittka B, Hadam M, Kreth H W. Measles virus infection causes transient depletion of activated T cells from peripheral circulation.. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology. 1999. DOI: 10.1016/s1386-6532(99)00002-5.

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