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HIV is a highly variable virus which mutates very readily. This means there are many different strains of HIV, even within
the body of a single infected person.
Based on genetic similarities, the numerous virus strains may be classified into types, groups and subtypes.
Group O appears to be restricted to west-central Africa and group N - a strain discovered in 1998 in Cameroon - is
extremely rare. In 2009 a new strain closely relating to gorilla simian immunodeficiency virus was discovered in a
Cameroonian woman. It was designated HIV-1 group P. 1 More than 90 percent of HIV-1 infections belong to HIV-1 group
M and, unless specified, the rest of this page will relate to HIV-1 group M only.
Within group M there are known to be at least nine genetically distinct subtypes (or clades) of HIV-1. These are subtypes
A, B, C, D, F, G, H, J and K. 2
Occasionally, two viruses of different subtypes can meet in the cell of an infected person and mix together their genetic
material to create a new hybrid virus (a process similar to sexual reproduction, and sometimes called "viral sex"). 3 Many
of these new strains do not survive for long, but those that infect more than one person are known as "circulating
recombinant forms" or CRFs. For example, the CRF A/B is a mixture of subtypes A and B.
The classification of HIV strains into subtypes and CRFs is a complex issue and the definitions are subject to change as
new discoveries are made. Some scientists talk about subtypes A1, A2, A3, F1 and F2 instead of A and F, though others
regard the former as sub-subtypes.
Subtype A and CRF A/G predominate in West and Central Africa, with subtype A possibly also causing much of
the Russian epidemic. 9
Historically, subtype B has been the most common subtype/CRF in Europe, the Americas, Japan and Australia
and is the predominant sub-type found among MSM infected in Europe. 10 Although this remains the case, other
subtypes are becoming more frequent and now account for at least 25 percent of new HIV infections in Europe.
Subtype C is predominant in Southern and East Africa, India and Nepal. It has caused the world's worst HIV
epidemics and is responsible for around half of all infections.
Subtype D is generally limited to East and Central Africa. CRF A/E is prevalent in South-East Asia, but originated
in Central Africa. Subtype F has been found in Central Africa, South America and Eastern Europe. Subtype G and
CRF A/G have been observed in West and East Africa and Central Europe.
Subtype H has only been found in Central Africa; J only in Central America; and K only in the Democratic
Republic of Congo and Cameroon.
As a Belgium study highlighted, local epidemics can be better understood if sub-types, patient demographics and
transmission routes are recorded. 11 Furthermore, the availability of this data can be used to target risk groups more
accurately and to improve the effectiveness of prevention strategies.
An HIV positive man sitting at home before taking his antiretroviral drugs
Although most current HIV-1 antiretroviral drugs were designed for use against subtype B, there is no compelling evidence
that they are any less effective against other subtypes. Nevertheless, some subtypes may be more likely to develop
resistance to certain drugs, and the types of mutations associated with resistance may vary. 39 This is an important
subject for future research.
The effectiveness of HIV-1 treatment is monitored using viral load tests. It has been demonstrated that some viral load
tests are sensitive only to subtype B and can produce a significant underestimate of viral load if used to process other
strains. 40 41 The latest tests do claim to produce accurate results for most Group M subtypes, though not necessarily for
Group O. It is important that health workers and patients are aware of the subtype/CRF they are testing for and of the
limitations of the test they are applying.
Not all of the drugs used to treat HIV-1 infection are as effective against HIV-2. 42 In particular, HIV-2 has a natural
resistance to NNRTI antiretroviral drugs and they are therefore not recommended. As yet there is no FDA-licensed viral
load test for HIV-2 and those designed for HIV-1 are not reliable for monitoring the other type. Instead, response to
treatment may be monitored by following CD4+ T-cell counts and indicators of immune system deterioration. 43 More
research and clinical experience is needed to determine the most effective treatment for HIV-2.
countries suggests that the effectiveness of a vaccine is likely to vary between populations, unless an innovative method is
developed which guards against many virus strains. 44
Inevitably, different types of candidate vaccines will have to be tested against various viral strains in multiple vaccine trials,
conducted in both high-income and developing countries.
References
expand >
Sources
UNAIDS Questions and Answers II, Section I, July 2004.
- See more at: http://www.avert.org/hiv-types.htm#sthash.5b7aZvdn.dpuf
Subtypes of HIV
Human
immunodeficiency virus
Virus classification
Group:
Group
VI
(ssRN
A-RT)
Family:
Retrovi
ridae
Genus:
Lentivi
rus
Species
Human
immunodeficiency
virus 1
Human
immunodeficiency
virus 2
International
Statistical
Classification of
Diseases and Related
Health Problems
Codes
Classification and external
resources
ICD-10
B2
0B2
4
ICD-9-CM
04
204
One of the obstacles to treatment of the human immunodeficiency virus is its high genetic variability.[1] HIV can be
divided into two major types, HIV type 1 (HIV-1) and HIV type 2 (HIV-2). HIV-1 is related to viruses found
in chimpanzees and gorillas living in western Africa, while HIV-2 viruses are related to viruses found in the
endangered west African primate sooty mangabey.[2] HIV-1 viruses may be further divided into groups. The HIV-1
group M viruses predominate and are responsible for the AIDS pandemic. Group M can be further subdivided into
subtypes based on genetic sequence data. Some of the subtypes are known to be more virulent or are resistant to
different medications. Likewise, HIV-2 viruses are thought to be less virulent and transmissible than HIV-1 M group
viruses, although HIV-2 is known to cause AIDS.
Major types
HIV-1[
HIV-1 is the most common and pathogenic strain of the virus. Scientists divide HIV-1 into a major group (Group M)
and two or more minor groups. Each group is believed to represent an independent transmission of SIV into
humans (but subtypes within a group are not).[2] A total of 39 ORFs are found in all six possible reading frames (RFs)
of HIV-1 complete genome sequence,[3] but only a few of them are functional.
Group M[]
With 'M' for "major", this is by far the most common type of HIV, with more than 90% of HIV/AIDS cases deriving
from infection with HIV-1 group M. The M group is subdivided further into clades, called subtypes, that are also
given a letter. There are also "circulating recombinant forms" or CRFs derived from recombination between viruses
of different subtypes which are each given a number. CRF12_BF, for example, is a recombination between subtypes
B and F.
Subtype B is the dominant form in Europe, the Americas, Japan, Thailand, and Australia. [5]
Subtype C is the dominant form in Southern Africa, Eastern Africa, India, Nepal, and parts of China. [5]
(Subtype E) has never been identified as a nonrecombinant, only recombined with subtype A as CRF01_AE.
[5]
Subtype F has been found in central Africa, South America and Eastern Europe. [6]
Subtype G (and the CRF02_AG) have been found in Africa and central Europe. [6]
(Subtype I) was originally used to describe a strain that is now accounted for as CRF04_cpx, with the cpx for
a "complex" recombination of several subtypes.[citation needed]
Subtype J is primarily found in North, Central and West Africa, and the Caribbean [7]
These subtypes are sometimes further split into sub-subtypes such as A1 and A2 or F1 and F2. [citation needed] In 2015, the
strain CRF19, a recombinant of subtype A, subtype D and subtype G, with a subtype D protease, was found to be
strongly associated with rapid progression to AIDS in Cuba.[8] This is not thought to be a complete or final list, and
further types are likely to be found.[9]
Group N[edit]
The 'N' stands for "non-M, non-O". This group was discovered in 1998 and has only been seen in Cameroon. As of
2006, only 10 Group N infections had been identified. [10]
Group O
The O ("Outlier") group is not usually seen outside of West-central Africa. It is reportedly most common in
Cameroon, where a 1997 survey found that about 2% of HIV-positive samples were from Group O. [11] The group
caused some concern because it could not be detected by early versions of the HIV-1 test kits. More advanced HIV
tests have now been developed to detect both Group O and Group N.[12]
Group P
In 2009, a newly analyzed HIV sequence was reported to have greater similarity to a simian immunodeficiency virus
recently discovered in wild gorillas (SIVgor) than to SIVs from chimpanzees (SIVcpz). The virus had been isolated
from a Cameroonian woman residing in France who was diagnosed with HIV-1 infection in 2004. The scientists
reporting this sequence placed it in a proposed Group P "pending the identification of further human cases". [13][14][15]
HIV-2
HIV-2 has not been widely seen outside of Africa. The first case in the United States was in 1987.[16] Many test kits
for HIV-1 will also detect HIV-2.[17]
As of 2010, there are 8 known HIV-2 groups (A to H). Of these, only groups A and B are epidemic. Group A spread
mainly in West Africa, but also to Angola, Mozambique, Brazil,India, and very limitedly to Europe or the US. Group B
is mainly confined to West Africa. [18][19]Despite its relative confinement, HIV-2 should be considered in all patients
exhibiting symptoms of HIV that not only come from West Africa, but also anyone who has had any body fluid
transfer with a person from West Africa (ie. needle sharing, sexual contact, etc.). [20]
HIV-2 is closely related to simian immunodeficiency virus endemic in sooty mangabeys (Cercocebus atys atys)
(SIVsmm), a monkey species inhabiting the forests of Littoral West Africa. Phylogenetic analyses show that the virus
most closely related to the two strains of HIV-2 which spread considerably in humans (HIV-2 groups A and B) is the
SIVsmm found in the sooty mangabeys of the Tai forest, in western Ivory Coast.[18]
There are six additional known HIV-2 groups, each having been found in just one person. They all seem to derive
from independent transmissions from sooty mangabeys to humans. Groups C and D have been found in two people
from Liberia, groups E and F have been discovered in two people from Sierra Leone, and groups G and H have
been detected in two people from the Ivory Coast. Each of these HIV-2 strains, for which humans are
probably dead-end hosts, is most closely related to SIVsmm strains from sooty mangabeys living in the same
country where the human infection was found.[18][19]
Diagnosis
HIV-2 diagnosis can be made when a patient has no symptoms but positive blood work indicating the individual has
HIV. The Multispot HIV-1/HIV-2 Rapid Test is currently the only FDA approved method for such differentiation
between the two viruses. Recommendations for the screening and diagnosis of HIV has always been to use enzyme
immunoassays that detect HIV-1, HIV-1 group O, and HIV-2.[20] When screening the combination, if the test is
positive followed by an indeterminate HIV-1 western blot, a follow up test, such as amino acid testing, must be
performed to distinguish which infection is present. [21]According to the NIH, a differential diagnosis of HIV-2 should be
considered when a person is of West African descent or has had sexual contact or shared needles with such a
person. West Africa is at the highest risk as it is the origin of the virus.
Treatments
HIV-2 has been found to be less pathogenic than HIV-1. The mechanism of HIV-2 is not clearly defined, nor the
difference from HIV-1, however the transmission rate is much lower in HIV-2 than HIV-1. Both infections can lead to
AIDS in affected individuals and both can mutate to develop drug resistance. [20] Disease Monitoring in patients with
HIV-2 includes clinical evaluation and CD4 cell counts, while treatment includes Anti-Retroviral Therapy (ART),
Nucleoside Reverse Transcriptase Inhibitors (NRTIs), Protease Inhibitors (PI), and Non-Nucleoside Reverse
Trascriptase Inhibitors (NNRTIs) with the addition of CCR5 co-receptor antagonists and fusion inhibitors. [22] Choice of
initial and/or second-line therapy for HIV-2 has not yet been defined. HIV-2 appears to be resistant to NNRTIs
intrinsically, but may be sensitive to NRTIs, though the mechanism is poorly understood. Protease inhibitors have
shown variable effect, while integrase inhibitors are also being evaluated. Combination regimens of the above listed
therapies are being looked into as well, also showing variable effect depending on the types of therapies combined.
While the mechanisms are not clearly understood for HIV-1 and HIV-2, it is known that they use different pathways
and patterns, making the algorithms used to evaluate HIV-1 resistance-associated mutations irrelevant to HIV-2.
[20]
Each virus can be contracted individually, or they can be contracted together in what is referred to as co-infection.
HIV-2 seems to have lower mortality rates than HIV-1 alone or the co-infection. In co-infection, however, this is
largely dependent on which virus was contracted first. HIV-1 tends to out compete HIV-2 for disease progression.
Co-infection seems to be a growing problem globally as time progresses, with most cases being identified in West
African countries, as well as some cases in the US.[22]
Pregnancy[
If a pregnant mother is exposed, screening is performed as normal. If HIV-2 is present, a number of perinatal ART
drugs may be given as a prophylactic to lower the risk of mother-to-child transmission. After the child is born, a
standard 6-week regimen of these prophylactics should be initiated. Breast milk may also contain particles of HIV-2;
therefore, breastfeeding is strictly advised against. [21]
Evolution
The AIDS virus is evolving to a milder form but is "an awfully long way" from no longer being deadly.[23]
Isolates of HIV-1 and HIV-2 with resistance to antiretroviral drugs arise through genetic mutations, which have been
tracked and analyzed. The Stanford HIV Drug Resistance Database and the International AIDS Society publish lists
of the most important of these; first year listing 80 common mutations, and the latest year 93 common mutations,
and made available through the Stanford HIV RT and Protease Sequence Database.