Given that more than 35 million people worldwide are infected with HIV and nearly 2 million new cases of HIV infection each year, the virus remains a major global epidemic. Existing antiretroviral drugs (ART) do not cure HIV infection because the virus can enter a dormant state and persist in the presence of immune cells. These infected immune cells (called latent virus banks) -- despite the use of ART drugs, remain in a latent state -- can be active again at any time.
Dr. Dan H. Barouch, director of the Virology and Vaccine Research Center at the Beth Israel Deaconess Medical Center, said, "This latent virus library is a key barrier to the development of a cure for HIV-1 infection. There is a hypothesis that activation of these latent viral pool cells may Make them more vulnerable to damage."
In a new study, Barouch and colleagues demonstrated that the combination of a broadly neutralizing agonistic antibody (bNAb) targeting HIV and a Toll-like receptor 7 (TLR7) agonist that stimulates the innate immune system can delay HIV cessation. Monkeys taking ART drugs rebounded. These findings suggest that this two-pronged approach represents a potential strategy for targeting this virus pool. The results of the study were published online October 3, 2018 in the journal Nature, entitled "Antibody and TLR7 agonist delay viral rebound in SHIV-infected monkeys".
Barouch and colleagues studied 44 rhesus monkeys infected with HIV-like virus (SHIV) and started treatment with ART for two and a half years after infection. After 96 weeks, these rhesus monkeys were divided into four groups. One group, the control group, did not receive any further study treatment. The other two groups were given only TLR7 antibody agonists or only bNAb antibodies. The fourth group was given both a TLR7 agonist and a bNAb antibody. All rhesus monkeys continued to receive ART medication until the 130th week of stopping the treatment, at which time the researchers began monitoring whether the rhesus monkeys showed signs of a rebound in SHIV.
As expected, in the control group, all rhesus monkeys rapidly rebounded with SHIV and they had a relatively high viral load peak, while in rhesus monkeys given only this TLR7 agonist, almost all The same is true for rhesus monkeys. However, among the rhesus monkeys receiving this combination therapy, 5 of the 11 rhesus monkeys did not rebound from the SHIV virus within 6 months. In addition, another 6 rhesus monkeys with SHIV virus rebound showed lower viral load peaks than rhesus monkeys in the control group. Rhesus monkeys given only bNAb antibodies showed detectable SHIV virus rebound, but this virus rebound was delayed.
"The combination of bNAb antibody and TLR7 agonist has led to the best killing of immune cells infected with SHIV," Barouch said. In summary, our data show that this combination therapy stimulates the innate immune system and allows infected cells to become more A mechanism that is easy to remove. T
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