HIV can cause serious inflammation, regardless of drug therapy, as it develops slowly in immune cells called macrophages. However, new research conducted at the Temple University School of Medicine’s Department of Pathology and Laboratory Medicine and Center for Substance Abuse Research (CSAR) has just found that there are synthetic agents with anti-inflammatory properties, related to the active ingredient in cannabis, THC (tetrahydrocannabinol) which could limit and treat the chronic inflammation.

According to new guidelines by the U.S. Preventive Services Task Force, published in the Annals of Internal Medicine, clinicians now recommend screening all patients aged 15 to 65, and other teens or older adults who are at an elevated risk for HIV infection.

HIV/AIDS is a serious pandemic, and current antiretroviral treatment options are effective at helping patients live longer. However, living longer with HIV is associated with inflammation, which can be the cause of HIV-associated neurocognitive disorder (HAND) according to the first author of the study, Servio H. Ramirez, PhD, Assistant Professor of Pathology and Laboratory Medicine at Temple University School of Medicine (TUSM).

HIV-associated neurocognitive disorder (HAND) occurs when HIV enters the nervous system and affects the nerve cells. It can result in attention, memory, and problem solving impairment. Symptoms of the condition include:

  • Headaches
  • Forgetfulness
  • Confusion
  • Pain because of nerve damage
  • Motor problems

Ramirez and team looked at a specific protein located on the surfaces of macrophages, called the CB2 receptor. The CB2 receptor acts as a binding site for the primary active compounds of cannabis, called cannabinoids. It could have the potential to block the inflammation which occurs in the central nervous system.

CB2 does not cause any of the psychoactive effects which are commonly associated with cannabis, making it unlike its counterpart, the CB1 receptor.

The researchers said that there has been overwhelming interest in making agents that target CB2. The compounds would help reduce inflammation and not bind to CB1.

The findings were published in the Journal of Leukocyte Biology.

Knowing which cells host HIV was crucial to this finding. The team focused on macrophage cells, which are a form of white blood cell that destroy foreign agents.

Macrophages are the main reservoir for HIV, according to the senior investigator of the study. They are one of the first cells to become infected after the virus enters the body. It is also thought that macrophages may well be the cause of HIV entering the brain, which causes mental impairment.

The team conducted numerous experiments in a non-clinical HIV macrophage cell model. They treated the HIV-infected cells with different types of CB2 activating agents. Following this, they regularly checked on the activity of transcriptase, an enzyme responsible for HIV replication. A week later all three agents had worked well at reducing HIV replication.

These findings suggest that CB2 agonists could be used along with antiretroviral drugs which could lead to a new form of therapy for HIV/AIDS.

It also suggests that the human immune system itself could be used to fight off the HIV infection.

According to Persidsky: “Our study suggests that the body’s own natural defenses can be made more powerful to fight some of the worst symptoms of HIV.”

Stimulating CB2 receptors could also be applied for treating other infections.

Persidsky concluded: “From our perspective we were in a better position for in vitro research. We have interesting models and were able to take advantage of our colleagues’ knowledge of receptors and cannabinoids to make a unique contribution.”

A remarkable recent study showed that 14 HIV-infected adults appeared to be “functionally cured” of HIV when they received antiretroviral drugs. Starting antiretroviral therapy during the “primary” stage of infection could be the key, because it appears to reduce viral reservoirs, preserve patients’ immune responses, and protect them from chronic immune activation.

Written by Joseph Nordqvist