Scientists have detected a new aggressive strain of human immunodeficiency virus (HIV) in Cuba that they say can progress to AIDS so rapidly that patients may not even know they are infected before symptoms appear. These findings were published in the journal EBioMedicine on January 28th.
Human Immunodeficiency Virus (HIV) infection causes a spectrum of conditions in patients ranging from initial influenza-like illness to debilitating conditions such as tuberculosis, and other opportunistic infections due to their weakened immune system. The late stages of infection is known as AIDS (or Acquired Immune Deficiency Syndrome) and can develop in typically 5-11years. HIV virus is primarily transmitted through unprotected sexual intercourse with an infected individual, from mother to her baby, or using shared needles etc.
Thus, having unprotected sex with multiple partners could increase the risk of contracting multiple strains of HIV from people, possibly causing these strains to recombine and turn into a new variant of the virus. And that is exactly what has happened today. Cuba has observed patients with one such recombinant HIV strain that is more aggressive than any other forms of HIV known till date. The patients typically progress from HIV infection to AIDS within three years of infection, compared to the usual 5-11 years.
Once the HIV virus enters the cell, it attaches to anchor points on the cell or co-receptors, which are proteins on the cell membrane. In the case of normal HIV strain infection, the virus uses the anchor point CCR5 and after many healthy years, it switches to the anchor point CXCR4 which signals a faster progression to AIDS. This was speculated to be the reason why the new strain is more aggressive than the previous known strains of HIV, as this transition occurs much faster.
Researchers at KU Leuven’s Laboratory for Clinical and Epidemiological Virology confirmed this theory and stated that the new strain of HIV virus detected in Cuban patients actually makes this transition much faster. Apparently the virus targets the anchor point CXCR4 early after infection, drastically shortening the healthy phase and triggering rapid progression to AIDS.
Professor Anne-Mieke Vandamme and an international team of researchers studied the blood of 73 recently-infected patients – 52 at AIDS diagnosis and 21 without AIDS- and compared results with blood from 22 patients who had progressed to AIDS after a normal healthy period with HIV.
When they analyzed samples of patients with the new strain of HIV (or recombinant HIV), they observed abnormally high doses of the virus and a molecule called RANTES. This molecule is an inherent part of our natural immune response and it exhibits its action by binding to CCR5 receptors. These CCR5 receptors are the usual anchor points to which most forms of HIV binds, before entering the cell. But now, due to the high concentration of RANTES in the blood, these CCR5 receptors are no longer available as anchor points for HIV. This causes, the recombinant HIV to bypass the usual route and directly attaches itself to the anchor point CXCR4, thereby leading to faster progression to AIDS. The observation that all study patients who were infected with the recombinant HIV variant went on to develop AIDS within three years of infection supports this theory.
The transition from anchor point CCR5 to CXCR4 is normally very difficult. The researchers suspect that the rapid transition observed in this HIV recombinant occurs as a result of combining fragments from different HIV subtypes. One of these fragments contains a protease (from subtype D), which acts very efficiently. Protease is an enzyme that cleaves the proteins that are used in new virus particles. This protease enables the virus to replicate in greater numbers hence facilitating the transition to CXCR4 anchoring.
One of the major concerns is that the unexpected rapid progression of this HIV variant increases the risk of those patients who are not aware of their condition, and may become very ill before ever realizing that they are infected.
The original publication can be read here.