HIV discovery could protect against 98% of strains

Dr Ben  Janaway  II  NOV 21 2016

Exciting new findings by researchers at the National Institute of Allergy and Infectious Disease have raised the prospect for almost universal treatment of HIV.  The antibody, named N6, utilized a unique approach interrupting the virus’ binding with our bodies immune cells, stopping the virus in its tracks. In testing, the team found that up to 98% of HIV1 strains were susceptible. These findings may lead to effective therapy and potential cure for the disease which still kills over a million a year.

Human Immunodeficiency virus effects our immune system, targeting our CDR helper t-cells and shutting down our defenses. The virus spreads through blood, either through sexual contract, childbirth, needle sharing and in rare cases, blood transfusions. Up to 0.05% of the UK are infected and 33% of these cases may be unaware of their diagnosis. Over time our body’s own immune system falters, rendering us susceptible to disease which is universally fatal if untreated.

Symptoms of infection include a mild flu type illness and rash, then a long wait of up to 10 years before increased rates of common infections becomes diagnostic.   At this point we are said to have an ‘Acquired Immunodeficiency Syndrome (AIDS), where usually harmless infections become lethal.

HIV is hard to treat due to its variable cell surface and variety of mutations, making it hard to target and kill with conventional therapy. It becomes through a process of cellular evolution ‘resistant’ to both bodily and drug defenses, making single drug treatments ineffective Current treatment is with a combination of anti-viral drugs. These drugs work together to prohibit resistance and suppress, but not kill, the virus overall.

Huang et al utilized a novel antibody to work within the V5 region of the HIV substructure, an area known to be fairly constant across all strains. By locking to the ‘CD4 binding site’, it was able to block infection of T-Cells (our bodies own watch-guards.) The team found that the N6 could bind regardless of tiny changes in the virus’ protein structure, allowing it a confluency not found in conventional treatments. It is this adaptation to the variable lineage of HIV that provides promise.           

This new pathway adds a robust plan of attack in a disease whose strength is change. Although we must wait for human trials and be aware that some strains will remain resistant, this new treatment offers great promise. Use in established HIV or as a prophylactic can only reduce the prevalence and effect of this still concerning infection.
HIV may one day become a thing of the past, whether through N6 or its progeny.

If you wish to learn more about HIV and donate toward research, visit the Terrance Higgins Trust

Any opinions above are the author's alone and may not represent those of Mind and Medicine. Any comment is based on the best available evidence at the time of writing.  All data is based on externally validated studies unless expressed otherwise. Novel data is representative of sample surveyed. Online recommendation is no substitute for seeing your own doctor and should not be taken as medical advice.


Hammond, A (2001) Antigenic variation within the CD4 binding site of Human Immunodeficiency Virus type 1 gp120: Effects on chemokine receptor Utlilization’

Huang et al (2016) Identification of a CD4- Binding Site Antibody to HIV that Evolved Near-Pan Neutralization Breadth ‘Immunity’ 45(5) p1108-1121   

Raja A et al (2003) CD4 binding site antibodies inhibit human immunodeficiency virus gp120 envelope glycoprotein interaction with CCR5 ‘ J Virol’  77(1) p 713-8

Simon, C et al (2016) ‘Oxford Handbook of General Practice’ 4th Edition, Oxford University Press, Oxford