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DOI 10.1016/j.bjid.2015.10.010

Медицинская библиотека · The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases · 2016

Toxoplasmic encephalitis: role of Human Leucocyte Antigens/alleles associated with rapid progression to Acquired Immunodeficiency Syndrome.

Rodrigues Maria de Lourdes, Deghaide Neifi Hassam, Figueiredo José Fernando, de Menezes Marcelo Bezerra, Demarco Ana Lúcia, Donadi Eduardo, Fernandes Ana Paula

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Аннотация

BACKGROUND/AIMS: The frequency of Human Leucocyte Antigens/alleles associated with rapid progression from Human Immunodeficiency Virus infection to Acquired Immunodeficiency Syndrome was evaluated in Brazilian patients with Acquired Immunodeficiency Syndrome with and without Toxoplasmic Encephalitis.

METHODS

114 patients with Acquired Immunodeficiency Syndrome (41 with Toxoplasmic Encephalitis, 43 with anti-Toxoplasma gondii antibodies, without Toxoplasmic Eencephalitis, and 30 without anti-Toxoplasma gondii antibodies circulating and without Toxoplasmic Encephalitis) were studied.

RESULTS

Human Leucocyte Antigens/alleles associated with rapid progression to Acquired Immunodeficiency Syndrome, particularly HLA-B35, -DR3, and -DR1 allele group, were significantly less represented in patients with Toxoplasmic Encephalitis and Acquired Immunodeficiency Syndrome.

CONCLUSION

The presence of these Human Leucocyte Antigens/Alleles that predispose to Acquired Immunodeficiency Syndrome progression was associated with resistance to Toxoplasmic Encephalitis among Human Immunodeficiency Virus-1 carriers.

Для цитирования: Rodrigues Maria de Lourdes, Deghaide Neifi Hassam, Figueiredo José Fernando, de Menezes Marcelo Bezerra, Demarco Ana Lúcia, Donadi Eduardo, Fernandes Ana Paula. Toxoplasmic encephalitis: role of Human Leucocyte Antigens/alleles associated with rapid progression to Acquired Immunodeficiency Syndrome.. The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases. 2016. DOI: 10.1016/j.bjid.2015.10.010.

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