并不是所有人都知道，HIV病毒不僅僅是一種,；除了常見(jiàn)的HIV-1型病毒外,，在非洲某些地方也發(fā)現(xiàn)了HIV-2型病毒。如今,，研究者發(fā)現(xiàn)已經(jīng)感染II型HIV的患者可以有效抵御I型HIV的感染,。相關(guān)研究成果刊登在了19日的國(guó)際雜志The New England Journal of Medical上。
II型HIV廣泛存在于西非的人群中,，研究者重點(diǎn)研究了223名首次感染II型HIV,，后感染I型HIV或者僅僅感染HIV-1的病人。通過(guò)跟蹤調(diào)查20年,，研究者表示,，已經(jīng)感染HIV-2的病人可以很好地處理并且應(yīng)對(duì)HIV-1的感染，因此對(duì)于獲得性免疫缺陷綜合癥有長(zhǎng)時(shí)間的疾病進(jìn)展時(shí)間,。
研究者目前首先研究?jī)H僅感染II型HIV的患者,，然而對(duì)于單獨(dú)感染I型HIV的病人來(lái)說(shuō)，其絕不可能感染II型HIV病毒,。HIV-2的感染可以緩慢地影響機(jī)體的健康，或許病毒的影響可以有效改善機(jī)體的免疫系統(tǒng),，以使得機(jī)體不在容易感染HIV-1,。（生物谷Bioon.com）
編譯自：HIV-2 infection inhibits HIV-1 disease progression
doi:10.1056/NEJMoa1113244
PMC:
PMID:
Inhibition of HIV-1 Disease Progression by Contemporaneous HIV-2 Infection
Joakim Esbjörnsson, Ph.D., Fredrik Månsson, M.D., Ph.D., Anders Kvist, Ph.D., Per-Erik Isberg, M.Sc., Salma Nowroozalizadeh, Ph.D., Antonio J. Biague, M.D., Zacarias J. da Silva, M.D., Ph.D., Marianne Jansson, Ph.D., Eva Maria Fenyö, M.D., Ph.D., Hans Norrgren, M.D., Ph.D., and Patrik Medstrand, Ph.D.
BACKGROUND Progressive immune dysfunction and the acquired immunodeficiency syndrome (AIDS) develop in most persons with untreated infection with human immunodeficiency virus type 1 (HIV-1) but in only approximately 20 to 30% of persons infected with HIV type 2 (HIV-2); among persons infected with both types, the natural history of disease progression is poorly understood. METHODS We analyzed data from 223 participants who were infected with HIV-1 after enrollment (with either HIV-1 infection alone or HIV-1 and HIV-2 infection) in a cohort with a long follow-up duration (approximately 20 years), according to whether HIV-2 infection occurred first, the time to the development of AIDS (time to AIDS), CD4+ and CD8+ T-cell counts, and measures of viral evolution. RESULTS The median time to AIDS was 104 months (95% confidence interval [CI], 75 to 133) in participants with dual infection and 68 months (95% CI, 60 to 76) in participants infected with HIV-1 only (P=0.003). CD4+ T-cell levels were higher and CD8+ T-cell levels increased at a lower rate among participants with dual infection, reflecting slower disease progression. Participants with dual infection with HIV-2 infection preceding HIV-1 infection had the longest time to AIDS and highest levels of CD4+ T-cell counts. HIV-1 genetic diversity was significantly lower in participants with dual infections than in those with HIV-1 infection alone at similar time points after infection. CONCLUSIONS Our results suggest that HIV-1 disease progression is inhibited by concomitant HIV-2 infection and that dual infection is associated with slower disease progression. The slower rate of disease progression was most evident in participants with dual infection in whom HIV-2 infection preceded HIV-1 infection. These findings could have implications for the development of HIV-1 vaccines and therapeutics. (Funded by the Swedish International Development Cooperation Agency–Swedish Agency for Research Cooperation with Developing Countries and others.) Supported by grants from the Swedish International Development Cooperation Agency–Swedish Agency for Research Cooperation with Developing Countries, the Swedish Research Council, the Crafoord Foundation, the Royal Physiographic Society, the Lars Hierta Memorial Foundation, Konsul Thure Carlsson Fund for Medical Research, the Tegger Foundation, the Medical Faculty of Lund University, and the regional agreement on medical training and clinical research between Region Skåne and the Medical Faculty of Lund University. We thank Françoise Barré-Sinoussi, Mattias Höglund, Mattias Mild, and Lisa Esbjörnsson-Klemendz for critically reviewing an earlier version of the manuscript; and Babetida N'Buna, Aquilina Sambu, Eusebio Ieme, Isabel da Costa, Jacqueline Pereira Barreto, Ana Monteiro Watche, Cidia Camara, Braima Dabo (deceased), Carla Pereira, Julieta Pinto Delgado, Leonvengilda Fernandes Mendes, Ana Monteiro, Ansu Biai, Fransisco Dias, Anders Nauclér, Gunnel Biberfeld, Sören Andersson, Helen Linder, Wilma Martinez-Arias, Pär-Ola Bendahl, and staff at the Swegene Center for Integrative Biology at Lund University for their contributions to this work. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. Drs. Esbjörnsson and Månsson contributed equally to this article.
