[Pre-exposure prophylaxis for HIV: clinical practice and challenge].

Antiretroviral therapy (ART) can not only turn HIV infection from a fatal disease into a treatable chronic disease, but also reduce HIV transmission among high-risk people. In recent years the concept "treatment as prevention" has been accepted by the public. More and more studies have shown that pre-exposure prophylaxis (PrEP) for HIV can effectively reduce the spreading of HIV in high-risk populations. Clinical trials have also shown that PrEP is safe, and can effectively prevent high-risk people from HIV infection. The guidelines of Europe, the United States and the World Health Organization (WHO) recommend that PrEP should be considered for high-risk populations including men who have sex with men (MSM), heterosexually active men and women, HIV-uninfected partner in serodiscordant couples and injection drug users(IDUs). PrEP with daily oral tenofovir/emtricitabine combination is the recommended PrEP regimen, and TDF alone can be considered as an alternative regimen for IDUs and heterosexually active adults. PrEP can provide a high level of protection against HIV, and is even more effective when it is combined with condoms, ART and other prevention methods. PrEP is currently facing great challenges including ethical issues, drugs accessibility, adherence, and low utilization rate, and should be further recommended for high-risk people to reduced HIV infection.

[Advances of immunological pathogenesis research in HIV related neurocognitive disorder].

With extended life of HIV-infected patients due to highly active anti-retroviral therapy (HAART), the rate of HIV associated neurocognitive disorder (HAND) remains high and attracts much attention. The evidence is clear that cytokines are elevated in the blood of patients with HIV infection, which contribute to elevating the permeability of blood-brain barrier. Benefiting from that, cells in the brain are infected with HIV that has accelerated through the blood-brain barrier both as cell-free virus and infected immune cells including monocytes and T cells. Upon migration into the central nervous system, HIV-infected monocytes and T cells not only infect brain resident cells but also produce proinflammatory cytokines such as TNF and IL-1ß, which further activate microglia and astrocytes. These activated brain glial cells and perivascular macrophages, which release inflammatory mediators, are the main contributors to neuroinflammation resulting in neuronal dysfunction. The pathogenesis of HAND is multifaceted, however, mounting evidence indicates that HIV related neuroinflammation plays a major role, which should be the focus of therapeutic research for HAND in future.