Each time HIV replicates (by infecting a new cell), small changes or mutations may occur.1 This means there are many different forms of HIV, including within the body of a single person living with HIV.
HIV-1 and HIV-2
HIV type 1 and HIV type 2 are two distinct viruses. Worldwide, the predominant virus is HIV-1, and generally when people talk about HIV without specifying the type of virus they are referring to HIV-1.
The relatively uncommon HIV-2 virus is concentrated in West Africa, but has been seen in other countries. It is less infectious and progresses slower than HIV-1. While commonly used antiretroviral drugs are active against HIV-2, optimum treatment is poorly understood.2 3
Groups within HIV-1
The strains of HIV-1 can be classified into four groups.4 The most important group, M, is the ‘major’ group and is responsible for the majority of the global HIV epidemic.
The other three groups are N, O and P. They are quite uncommon and only occur in Cameroon, Gabon and Equatorial Guinea.
Subtypes within HIV-1 group M
Within group M there are known to be at least nine genetically distinct subtypes of HIV-1. These are subtypes A, B, C, D, F, G, H, J and K.
Additionally, different subtypes can combine genetic material to form a hybrid virus, known as a ‘circulating recombinant form’ (CRFs), of which quite a few have been identified.5
The dominant HIV subtype in the Americas, Western Europe and Australasia is subtype B. As a result, the great majority of HIV clinical research has been conducted in populations where subtype B predominates. However this subtype represents only 12% of global HIV infections.
In contrast, less research is available for subtype C, although just under half of all people living with HIV have subtype C. It is very common in the high prevalence countries of Southern Africa, as well as in the horn of Africa and India.
The greatest diversity of subtypes is found in Cameroon and the Democratic Republic of Congo - the region where the HIV-1 epidemic originated.
However, these geographical patterns in the distribution of subtypes are changing over time, due to migration and the mixing of populations.6
Do differences in subtypes matter?
Some studies suggest that certain subtypes have a greater risk of transmission or faster disease progression than others.7 On the other hand, antiretroviral drugs (ARVs), although largely developed in relation to subtype B, have generally proven to be effective against a wide range of subtypes.8 9
Nonetheless, comparative research on these important issues is relatively limited, partly because individuals with different subtypes are found in distinct geographical locations.
A more practical concern are the tests used to diagnose HIV and monitor the level of virus in the body (viral load). Tests that are sensitive to the full range of subtypes (and to group O and HIV-2) do exist but may not be readily available in all settings. This is a concern in places where diverse subtypes are prevalent.
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- 1. Smyth, R.P. et al (2012) ‘The origin of genetic diversity in HIV-1’ Virus Research 169(2):415-429
- 2. Campbell-Yesufu, O.T. & Gandhi, R.T. (2011) ‘Update on human immunodeficiency virus (HIV)-2 infection’ Clinical Infectious Diseases 52(6):780-787
- 3. Ekouevi, D,K. et al (2014, August) ‘Antiretroviral therapy response among HIV-2 infected patients: a systematic review’ BMC Infectious Diseases 14:461
- 4. Hemelaar, J. (2012, March) ‘The origin and diversity of the HIV-1 pandemic’ Trends in Molecular Medicine 18(3):182-192
- 5. Hemelaar, J. (2012, March) ‘The origin and diversity of the HIV-1 pandemic’ Trends in Molecular Medicine 18(3):182-192
- 6. Fox, J. et al (2010) ‘Epidemiology of non-B clade forms of HIV-1 in men who have sex with men in the UK’ 24(15):2397-2401
- 7. Pant Pai, N. et al (2012) ‘Does genetic diversity of HIV-1 non-B subtypes differentially impact disease progression in treatment-naive HIV-1-infected individuals? A systematic review of evidence: 1996-2010’ JAIDS 59(4):382-388
- 8. Geretti, A.M. et al (2009) ‘Effect of HIV-1 subtype on virologic and immunologic response to starting highly active antiretroviral therapy’ Clinical Infectious Diseases 48(9):1296-1305
- 9. Rami, K. (2006) ‘Impact of HIV-1 pol diversity on drug resistance and its clinical implications’ Current Opinion in Infectious Diseases 19(6):594–606