Researchers at Johns Hopkins found that a safe and inexpensive antibiotics commonly used to treat acne since the 1970s can make HIV or the virus that causes AIDS was asleep and prevent virus reactivation and replication.Antibiotic drug called minocycline may improve current treatment regimens for HIV-infected patients when used in combination drug standards based HAART (Highly Active Antiretroviral Therapy). The new research published online this will be printed in the Journal of Infectious Diseases edition April 15.
Strong profits using minocycline is that the virus that appears less so that they can develop drug resistance because minocycline is a target in the cell lines rather than viral proteins, says Janice Clements, Ph.D., vice dean of faculty and professor of molecular and Comparative Pathobiology at the Johns Hopkins University School of Medicine, as quoted from MedicalNewsToday.
According to Clements, a big challenge when treating patients with HIV is the virus that remains locked in the inactive state. ART (Antiretroviral Therapy) really effective damping replication (duplicate) active, minocycline is another way to defense against viruses.
Unlike drugs used in therapy that targets the virus, the target of minocycline is immune cells known as T cells According to Clements, minocycline reduces the ability of T cells to the active and multiply, two important steps in the production and development of HIV into AIDS.
ART usually can protect people with HIV from the hospital, but it was not a drug. HIV virus is maintained at a low level but never fully cleared. The virus is still secretly lurking on immune cells. If a person stops taking HAART or miss a dose, the virus can be active again, out of the cells and the immune system began to spread.
The idea for using minocycline in addition to HAART appears when Hopkins research team conducts research on rheumatic patients who showed anti-inflammatory effects of minocycline on T cells.
Tim Hopkins connects with previous studies, which showed that minocycline treatment has many beneficial effects on SIV-infected monkeys, the primate version of HIV. Monkeys treated with minocycline, the virus load in cerebrospinal fluid and viral RNA in the brain significantly decreased. It also shows the influence of activation and proliferation of T cells.
Because minocycline can reduce T cell activation, you might think it would harm the immune system in monkeys, which is very similar to humans, but we did not see adverse effects, said Gregory Szeto, a graduate student in the Department of Cellular and Molecular Medicine who worked at the Retrovirus Laboratory Hopkins.
He thinks these drugs in a good balance, and ideal for HIV because the target is very specific aspects of immune system activation.
The success of the monkey studies encourage the team to learn whether minocycline treatment effect on latency in human T cells infected by HIV. The team uses human cells infected with HIV on HAART, isolated immune cells are "resting" and treated with minocycline half.
"Minocycline reduces the ability of the virus to exit infected T cells are resting," Szeto. This prevents the virus to escape on the person using ART, and therefore can prevent activation of the virus, to maintain the level of viral latency or even lower.
