Study identifies a protein critical for HIV infection

View:211 Time:2017-12-04

HIV infection rates have increased in many countries in the latest several decades, according to recent reports. The precise mechanisms by which the virus infects host cells and evades the host's immune attacks have not been fully understood, despite numerous attempts by scientists worldwide.

Currently, there is no HIV vaccine yet, increasing the difficulty of HIV prevention. The use of antiretroviral therapy (ART) has greatly improved life quality of and extended the lives of HIV-positive people, but ART does not cure HIV infection and may cause various short-term and long-term side effects. Once HIV-positive people start ART treatment, they generally have to take ART drugs every day for the rest of their life. If they stop taking these drugs, the HIV virus may return to pre-treatment levels and result in a loss of CD4 cells.

A new study (Bicaudal D2 facilitates the cytoplasmic trafficking and nuclear import of HIV-1 genomes during infection) shed light on how HIV manages to enter the nucleus of infected cells. The study was carried out by Adarsh Dharan, Omar Abdel-Rahim, Sevnur Komurlu Keceli, Sabrina Imam, and Edward Campbell from Loyola University Chicago, as well as Silvana Opp and Felipe Diaz-Griffero from Albert Einstein College of Medicine. The full paper can be read in the Proceedings of the National Academy of Sciences (PNAS).

Like other viruses, HIV cannot multiply on its own. HIV infects and kills key cells in the immune system, such as macrophages and T cells. When these immune cells are reduced, the body is less capable of fighting diseases and infections. In the HIV life cycle, HIV attaches to a target cell, fuses with it, takes control of it, replicates and releases new HIV. Many related viruses get into the nucleus of the target cell by waiting until cell divides. HIV, however, is able to enter the nucleus in a non-dividing cell. The cytoplasm of human cells is a solution full of organelles and other substances. Why does HIV travel through the cytoplasm to the nucleus so quickly?

A lot of works have been done to solve this mystery. Earlier studies have suggested that HIV-1 and many other viruses move toward the nucleus by using microtubules as a conduit. Microtubules are cytoskeletal structures found throughout the cytoplasm. Specifically, HIV-1 uses dynein, a family of cytoskeletal motor proteins that move along microtubules, to facilitate the delivery of the viral genome to the nucleus of the cell.

In this work, Campbell and other researchers found that BICD2, a known dynein adaptor protein, could interact with HIV-1 viral cores and promote the trafficking of HIV-1 to the nucleus of target cells. Further, they discovered that depletion of BICD2 sensitized the virus to detection by innate immune sensing. Taken together, the data suggest that BICD2 facilitates the trafficking of HIV-1 in the cytoplasm of target cells and helps the virus evade innate sensing mechanisms in target cells. Thus, preventing HIV-1 from interacting with BICD2 presents a potential strategy to prevent the virus from moving to the nucleus and suppress infection.

To develop preventive and therapeutic strategies, understanding how HIV infection is established is essential. This study would lead to more effective treatments for HIV and AIDS.
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