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Increased risk of developing peripheral neuropathy in patients coinfected with HIV-1 and HTLV-2.

作者信息

Zehender Gianguglielmo, Colasante Chiara, Santambrogio Sara, De Maddalena Chiara, Massetto Benedetta, Cavalli Barbara, Jacchetti Gaia, Fasan Marco, Adorni Fulvio, Osio Maurizio, Moroni Mauro, Galli Massimo

机构信息

Istituto di Malattie Infettive e Tropicali, Università degli Studi di Milano, Milan, Italy.

出版信息

J Acquir Immune Defic Syndr. 2002 Dec 1;31(4):440-7. doi: 10.1097/00126334-200212010-00011.

Abstract

One thousand one hundred fifty-two HIV-1-positive patients were screened for HTLV-2 infection, and the AIDS-free coinfected individuals were consecutively included in a longitudinal study with the aim of investigating the role of HTLV-2 in the progression to AIDS and the development of specific neurologic diseases. Two matched HIV-1-positive/HTLV-2-negative controls for each coinfected individual were also enrolled in the study. HTLV-2 infection was found in 95 (8.2%) of the HIV-1-positive patients, 30 of whom were followed up for a median of 28.5 months. No significant differences were observed between them and the patients infected with HIV-1 alone in terms of the rate of decline in CD4 cell counts, progression to AIDS, or AIDS mortality, but they had an increased risk of developing peripheral neuropathy (hazard ratio, 3.3; 95% confidence interval, 1.3-8.0; p =.009). One coinfected patient developed myelopathy during the follow-up. In the second part of the study, aimed at preliminarily assessing the effect of highly active antiretroviral therapy (HAART) on the incidence of peripheral neuropathy, we extended our observations to two groups of coinfected and singly infected individuals receiving HAART. An 80% decrease in incidence of peripheral neuropathy was observed among both groups without any significant difference between them. These results support the hypothesis that HTLV-2 plays a role in the development of neurologic abnormalities in HIV-1-infected patients and suggest that the immune reconstitution due to HAART may limit the activity of HTLV-2 as an opportunistic agent.

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