The last two days of the conference saw promising news for eradication research. Yesterday, Sarah Palmer from the Karolinska Institute in Sweden reported that she and her colleagues compared single HIV RNA sequences from plasma taken from eight patients just days before they started HAART, with sequences of single integrated proviral HIV DNAs in T cells from the same patients’ blood and gut associated lymphoid tissue (GALT) taken between four and ten years later.

So far the only person believed to have been cured from HIV infection is Timothy Brown, after receiving a number of anti-cancer treatments and eventually a stem cell transplant to treat acute myeloid leukemia. The stem cells came from a donor who was homozygous for the so-called CCR5Δ32 allele, which abrogates expression of the HIV co-receptor CCR5 on cells (see In Pursuit of a Cure, IAVI Report, Jan.-Feb. 2012). 

The HIV reservoir in latently HIV infected cells is considered one of the major remaining obstacles for eradication of HIV. Researchers hope to treat HIV infected patients who are receiving antiretroviral therapy (ART) with drugs that induce HIV expression in latently infected cells so that they can then try to remove or kill those cells. 

HIV can be transmitted as a free particle, or from cell to cell, for example between CD4+ T cells, through so-called virological synapses. One question is why HIV particles are budding preferentially in such synapses. At today’s session on retroviral entry mechanisms, Clare Jolly from the University College London reported that the reason seems to be that the cell-cell contact induces polarization of the infected donor cell, in that the microtubule organizing center migrates towards the site of cell-cell contact. This suggests that HIV proteins probably migrate along microtubules towards the virological synapse, which could explain why HIV particles preferentially bud there. 

This year’s Keystone meeting on HIV Pathogenesis, Therapy and Eradication, which takes place in Whistler, British Columbia from March 26-31, is held jointly with a meeting on Virus Entry, Replication and Pathogenesis, which includes discussion of many viruses other than HIV. The idea of this combination is to strengthen the interaction between HIV researchers and researchers who work on viruses other than HIV, said Michael Farzan, a virologist from Harvard Medical School and one of the organizers of the Virus Entry, Replication and Pathogenesis track. “I hope that what will happen is that more than usual, ideas from virology go to HIV virology, and ideas from HIV virology go to the more conventional virology,” Farzan said, “because HIV researchers frequently reinvent wheels that other virologists have done, but on the other hand HIV is also frequently ahead because [it is] the most studied virus.”