An uncommon use for a common drug offers hope to millions of HIV-positive patients

By Liz H. ‘10

Microscopic view of HIV (green) emerging from an infected T-cell. CDC

A promising new HIV treatment has been discovered in an unlikely source:  a widely available acne medication developed in the 1970s.  A team of scientists from Johns Hopkins University reports that minocyclin stops HIV-infected human cells from reactivating and replicating, in a study published in the April 15th issue of the Journal of Infectious Diseases.  Their findings may lead to an improved and more effective treatment regimen for HIV infection.

The researchers focused their study on latent, non-replicating HIV-infected human T-cells.  T-cells are a type white blood cell that normally fights infection.  HIV infects T-cells and can “rest” inside of them for an extended period of time.  The virus does not harm the T-cell during this latent phase, but can eventually “wake-up” and re-activate the T-cell, which spreads HIV infection and weakens the immune system.

In this study, the scientists treated latent HIV-infected human T-cells with minocycline and measured the level of re-activated T-cells over time.  They also performed the same measurements on cells that were not treated with minocycline.  The researchers found that the minocycline-treated cells did not display detectable levels of reactivation while the untreated cells displayed elevated levels.

Upon closer analysis of the activity of minocycline inside of cells, the scientists discovered that the drug interferes with important cellular communication pathways that cause the T-cell to activate and spread HIV to other cells.  “It prevents the virus from escaping in the one in a million cells in which it lays dormant in a person…That’s the goal:  Sustaining a latent non-infectious state,” explains Gregory Szeto, a Hopkins graduate student who worked on the project.

These findings suggest that minocycline could be used in conjunction with HAART, the current HIV treatment standard, to keep the virus dormant inside of T-cells.  “While HAART is really effective in keeping down active replication, minocycline is another arm of defense against the virus,” says author Janice Clements.  Minocycline is an attractive addition to the current arsenal of HIV medications because it is relatively inexpensive, does not inhibit the ability of T-cells to fight other infections, and is not likely to cause viral drug resistance.

Current treatment for HIV/AIDS involves a combination therapy approach known as HAART.  Patients on HAART take at least 3 antiretroviral drugs daily that act on the virus in different ways to reduce its levels in the bloodstream.  Although HAART can extend the life of an infected individual, it is not a cure and causes unpleasant side effects and the development of drug resistance.  For the 40 million HIV-positive individuals worldwide, this new use for minocycline promises improved outcomes.

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Press Release

What Doesn’t kill Them Makes Them Stronger

By Nick Gubitosi         February 13, 2010

This past Thursday, a group of scientists from Boston University released a new study which revealed that treating bacteria with low levels of antibiotics produces mutations in the bacteria instead of killing them, allowing them to gain resistance to a wide range of antibiotics.  This newly gained understanding for the biomolecular processes that produce these “superbugs” can lead to the development of new antibiotics or even enhanced treatments that could prevent the creation of these extremely dangerous cross-resistant bacteria.

The team of scientists led by Professor James Collins, performed their tests on strains of E. coli and Staphylococcus.  They started by administering low levels of five different antibiotics to the bacteria, which caused the introduction of mutations into the bacterial DNA.  They followed this by then giving lethal doses of antibiotics to these mutated bacteria.  The results revealed that many of the bacteria initially exposed to low levels of antibiotics now exhibited cross-resistance to a variety of antibiotics.

In lethal levels, antibiotics cause bacterial DNA to be shredded.  However, when the antibiotic is not at a lethal level, mutations are entered into the bacterial DNA instead.  The bacteria not only survive with these mutations, but gain protection from antibiotics including ones that the bacteria weren’t even exposed to.

This study helps to show the serious dangers involved with taking low or incomplete doses of antibiotics, which is common practice in many areas today.  Farmers who include antibiotics in their livestock feed, doctors who prescribe antibiotics at random, and patients who don’t follow their full course of drugs are all promoting the creation of these bacterial “superbugs.”

With the information gained from these findings, enhanced antibiotic treatments can be developed that could prevent the emergence of multi-drug resistant bacteria and even increase their DNA killing ability so that low doses of antibiotics would be enough to kill mutated bacterial cells.

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