Laboratoire Retrovirus, IRD, 911 Avenue Agropolis, BP5045, 34032 Montpellier, France
e-mail : email@example.com
One of the major characteristics of the human immunodeficiency viruses (HIVs) is their extremely high genetic variability. This extensive heterogeneity is the result of the high error rate of reverse transcriptase , and the fast turnover of virions in HIV-infected individuals (32, 107]. In addition, the reverse transcriptase enzyme is known to be highly recombinogenic , so that radically different genomic combinations may be generated in individuals infected by genetically diverse viruses. Recombination requires the simultaneous infection of a cell with two different proviruses, allowing the encapsidation of one RNA transcript from each provirus into a heterozygous virion. After the subsequent infection of a new cell, the reverse transcriptase, by jumping back and forth between the two RNA templates, will generate a newly synthesized retroviral DNA sequence that is recombinant between the two parental genomes (28, 35, 94].That mosaic viruses are indeed recombinants is supported by the fact that discrete breakpoints can be identified between the genomic regions with different phylogenetic associations [13, 23]. It is now well established that recombination is a relatively common occurrence among different strains of HIV [reviewed in 77]. Recombination is most obvious among members of different subtypes, and is also likely to occur among members of the same subtype, although current methods fail to reliably identify such intra-subtype recombination.
Classification of HIV-1 strains
Phylogenetic analyses of numerous strains of HIV-1, isolated from diverse geographic origins, have revealed that they can be subdivided into groups, subtypes, sub-subtypes and CRFs [81, 82, 83, 103], see Figure 1.
Groups refer to the very distinctive HIV-1 lineages M, N and O. The vast majority of HIV-1 strains found worldwide and responsible for the pandemic, belong to just one of these lineages, group M (for Major). Group O seems to be endemic to Cameroon and neighboring countries in West Central Africa, but even there these viruses represent a minority of HIV-1 strains: their highest prevalence is 2-5 of HIV-1 positive samples [55, 71, 113]. Group N (for New, or non-M, non-O) has only recently been identified, and is so far represented by a limited number of isolates from Cameroonian patients [7, 91].
Within group M, there is further phylogenetic structure, allowing the classification of HIV-1 M strains. Subtypes were proposed because most sequences of group M were found to fall into a limited number of discrete clades [51, 52]. The subtypes are approximately equidistantly related and in order to be considered as a subtype, isolates should resemble each other, and no other existing subtype, across the entire genome. In this light, there are only nine subtypes of HIV-1 group M, (A-D, F-H, J and K). In the case of subtype G, there is some ambiguity about the origins of the accessory gene region, which is close to subtype A [13, 23, 83], however, most of the subtype G genome is phylogenetically distinct. Phylogenetic analyses of group O strains have not revealed the same substructure as found within the evolutionary tree of group M, and so this group has not been classified into subtypes.
Within some subtypes, further phylogenetic structure can be identified, leading to a classification into subclades. subtype F is subdivided into 2 subclades, F1 and F2  and it is clear that subtypes B and D would be better considered as subclades of a single subtype, but for historical reasons it is difficult
Figure 1. Evolutionary relationships among non-recombinant HIV-1 strains from the HIV-1/SIVcpz lineage, based on neighbor joining phylogenetic analysis of near full length genome sequences. The phylogenetic tree shows the different HIV-1 groups, subtypes and sub-subtypes. Each of the internal branches defining a subtype or sub-subtype is supported by 100 of bootstraps.
to change these designations. Also within subtype A, sub-subtype A2 strains have been recently described .
Subsequent to the designation of group M subtypes, it was realized that certain isolates clustered with different subtypes in different regions of their genomes when phylogenetic analyses were performed . Some of these mosaic HIV-1 genomes have been identified in several, apparently unlinked, individuals and play a major role in the global AIDS epidemic and are now designated as "Circulating Recombinant Forms", or CRFs . Members of a CRF should resemble each other over the entire genome, with similar breakpoints reflecting common ancestry from the same recombination event(s). There are currently several CRFs of HIV-1: under new nomenclature proposals, each will be designated by an identifying number, with letters indicating the subtypes involved . If the genome contains sequences originating from more than two subtypes, the letters will be replaced by "cpx", denoting "complex".
In order to define a new subtype, sub-subtype or CRF, representative strains must be identified in at least three individuals with no direct epidemiological linkage. Three near full-length genomic sequences are preferred, but two complete genomes in conjunction with partial sequences of a third strain are sufficient to designate a new subtype, sub-subtype or CRF (to define a CRF, the partial sequence(s) must also confirm the CRFs mosaic structure).
The different CRFs, actually known are summarized in Table 1 and Figure 2 shows the complex mosaic genomic structure for each of them
Table 1. Summary of the defined Circulating Recombinant Forms (CRF) of HIV-1 group M
name subtypes involved geographic distribution
CRF01-AE A, E predominant in Southeast Asia, sporadic in Central Africa
CRF02-AG A, G predominant in West and West Central Africa
CRF03-AB A, B Russia (Kaliningrad)
CRF04-cpx A, G, H, K, U Greece, Cyprus
CRF05-DF D, F Democratic Republic of Congo
CRF06-cpx A, G, J, K West Africa (Mali, Senegal, Nigeria, Burkina Faso, Niger)
CRF07-BC B, C northwest China
CRF08-BC B, C southeast China
CRF09-cpx unpublished Senegal, US
CRF10-CD C, D Tanzania
CRF11-cpx A, E, G, J Central Africa (Cameroon, Central African Republic, Gabon)
All known representatives of what was initially described as subtype E appear in fact to be recombinants of subtypes A and E [12, 22], and are now designated CRF01-AE . subtype E was first designated on the basis of the distinct phylogenetic position of these viruses in env trees, the only non-subtype A sequences are found within (most of) the env gene, parts of vif, vpr and nef, and the LTR. A full length non-recombinant subtype E sequence has not yet been described and the absence of one of the "parental" lineages leads to difficulties in formally proving the recombinant nature of these viruses . CRF01-AE viruses have been documented at low frequencies in several Central African countries, like Central African Republic, Cameroon and the Democratic republic of Congo [64, 66, 105], but they are responsible for the explosive epidemic in Southeast Asia, especially in Thailand from where these viruses have further spread to surrounding countries like Vietnam, Cambodia, Myanmar and China [42, 58, 59, 62, 75, 108].
The IbNg strain from Ibadan, Nigeria, was initially described as a divergent lineage within subtype A, based on gag and env sequences . However, after the determination of a full length sequence, IbNg was recognized as a complex mosaic of alternating subtype A and subtype G sequences . Since a number of similar viruses have been reported from countries in both West and East Africa, this clade is now designated as CRF02-AG. CRF02-AG is the predominant HIV-1 strain in West and West Central Africa, where they represent between 50% to 70% of the circulating strains [4, 56, 61, 67, 73, 98]. These viruses have now also been introduced in Europe and to a minor extent in the US [18, 57].
Figure 2. Schematic representation of the complex mosaic genomic structure from the actually published circulating recombinant forms (CRFs).
An epidemic among intravenous drug users (IDUs) in Kaliningrad, Russia, involves viruses that are mosaics of subtypes A and B [9, 48], and so are termed CRF03-AB. Subtype A and B strains from Ukranian IDUs were shown to be the probable parental viruses of the Kaliningrad AB recombinant strain . The epidemic in Kaliningrad was explosive and large numbers of simultaneous infections with this particular HIV-1 variant occurred, offering a unique opportunity to study the virus in a setting where the epidemic was captured in the earliest stages of spreading.
Isolate 94CY032 from Cyprus was designated as the prototype of subtype I based on gp120 sequences . However, full genome sequencing revealed this virus was a complex recombinant with A, G and a putative new subtype, I. Multiple breakpoints were observed between the distinct subtypes  and two similar viruses have been reported from epidemiologically unlinked individuals from Greece . Re-analysis with previously unavailable complete genome sequences revealed that some of the unknown regions were in fact subtype H or K, but still some regions could not be classified. Thus, subtype I was removed from the genetic classification system of HIV strains, and the "I" regions were relabelled as unclassified (U). These strains are now called CRF04-cpx, and their genome is comprised of subtype A, G, H, K and unknown fragments with multiple breakpoints [83, 88].
Two full-length strains were shown to be mosaics of subtypes F and D, CRF05-DF. These epidemiologically unrelated FD sequences showed similar chimeric structure and partial sequences from three additional unlinked FD recombinants confirmed this. Genetic distances in the phylogenetic trees suggest that the recombination event leading to the putative CRF occurred relatively long ago. Furthermore, all five FD recombinants are linked to the Democratic Republic of Congo, suggesting that the original recombination event took place in central Africa [47 ].
Two near-full-length genomes of similar complex mosaic viruses, containing fragments of (at least) subtypes A, G and J, have recently been described in patients from Burkina Faso (BFP90) and Mali (95ML84) [60, 68]. Phylogenetic and recombinant analysis from two additional full-length genome sequences from epidemiologically unlinked individuals, one from Senegal (97SE-1078) and one from Mali (95ML-127), had a similar mosaic structure and confirmed that the previously described strains, BFP90 and 95ML84, represent a new CRF of HIV-1, designated as CRF06-cpx, since 4 different subtypes were involved in the mosaic genome structure. This new CRF was composed of successive fragments of subtype A, G, K and J. The fragment in the pol gene that was initially characterized as unknown in the BFP90 strain and subsequently as subtype I in the 95ML84 strain, was now clearly identified as subtype K. CRF06-cpx circulates in Senegal, Mali, Burkina Faso, Ivory Coast, Niger and Nigeria, although the exact prevalences remain to be determined (Toure Kane C, Montavon C, Nkengasong J, Saidou M, Peeters M, personal communication). Importantly, this new variant was also introduced in other continents, Europe (France) and Australia, showing that these viruses are present not only locally but also globally. [68, Montavon C, Peeters M, personal communication].
Two different BC recombinants have been detected in intravenous
drug users (IDU) in China. CRF07-BC, with the 97CN-54 prototype
strain, are isolated among IDUs in the northwestern part of
China . CRF08-BC, prototype 97CN-6F, is documented in IDU in Guangxi, southern China neighboring Myanmar  . CRF08-BC strains are mostly subtype C with portions of the capsid and reverse transcriptase genes from subtype B. Whereas the breakpoint in p24/p17 and the RT gene overlap, CRF07-BC strains have additional breakpoints in the p7/p6 genes, the vpr/vpu, and in the 3' portion of nef. The two parental B-Thai and C subtypes have been reported earlier to co-circulate among IDUs in southwestern China, therefore clearly representing a potential reservoir for recombination [29, 53, 111, 112]. Two different routes of BC recombinants spread throughout China, suggesting different founder effects in the Chinese IDU population .
CRF09-cpx has been described in Senegal and a US military seroconverter . CRF10-CD was recently described in a cohort studying mother to child transmission of HIV-1 in Dar-es-Salaam, Tanzania . In this country, subtypes A, C and D cocirculate in equal proportions and many samples with discordant subtype designations between 2 or more genomic regions have already been documented [33, 79, 80]. CRF11-cpx, involving subtypes A, G, J and E is observed in Cameroon and the Central African Republic (CAR). These strains were also described in individuals in Europe, but infected with HIV overseas, more precisely in Djibouti, CAR and even in French Guyana. A recently reported A, G, E, ? strain, isolated from a patient in Greece, seems after reanalysis of the genome, to have a similar mosaic structure as CRF11-cpx. [70, 101, Montavon C, Peeters M, personnel communication)
The majority of CRFs have been documented in local epidemics only. This is the case for CRF03-AB, CRF04-cpx, CRF05-DF, CRF07-BC, CRF08-BC, and CRF10-CD. Some are spreading into different countries, but actually their prevalence seems to be low, like CRF06-cpx, CRF09-cpx and CRF11-cpx. CRF01-AE and CRF02-AG, however, account for large numbers of HIV-1 infections worldwide, and play a major role in the global epidemic, in southeast Asia and Africa respectively, and they are also introduced to other continents.
In addition to all this circulating recombinants, full-length genome sequences from many more unique recombinants have been described. Several AC and AD recombinants have been described in Eastern Africa [14, 45, 57, 87], where these 3 subtypes co-circulate. BF recombinants have been found in Brazil and Argentina, where subtypes B and F are both common [54, 84, 85]. Subtypes A and C co-circulate in India, and AC recombinants are present [37, 50]. Recently, a B/CRF01-AE was observed in Thailand were subtype B and CRF01-AE were initially introduced .Various other complex recombinants including even small or large fragments from unclassified sequences have been reported from Africa where all subtypes cocirculate. In addition, some of the first African HIV-1 isolates to be characterized, MAL and Z321(obtained from a stored plasma sample obtained in 1976 in a rural area in the north of the DRC , have been identified as complex recombinants, AD? and AG? respectively [2, 16]. Some of the unknown fragments can be present in two different recombinants. For example, the 97CD-KTB49 strain from DRC is a complex recombinant involving subtypes A, E, G, H, J, K and unknown fragments in the vif-vpr region . Additional analyses confirmed also that the vif-vpr fragments consists of 2 different unknown fragments with the 5 end of the vif gene corresponding to the unknown fragment of the Z321 strain and the 3 end of the vif and the vpr fragment corresponding to the unknown fragment common between Z321 and CRF04-cpx. Another example is the NOGIL3 virus from a family in Norway , where some of the unclassified fragments correspond to unknown fragments observed in the Mal virus. Figure 3 illustrates the complex genomic structure of these viruses mainly from Central African origin. The presence of recombinant viruses early in the AIDS epidemic and the complexity, as well as the numerous unclassified fragments found in recombinants that actually circulate in Central Africa, confirms that HIV was already present for a while in this region of Africa.
Figure 3. Schematic representation of the complex mosaic genomic structure from unique recombinant HIV-1 viruses of Central African origin. This figure illustrates that some unclassified fragments can be present in different recombinant viruses.
Recombination between HIV groups
It was initially suspected that homologous recombination between group M and group O viruses may not be possible because of their high degree of divergence. Two recent reports however have documented intergroup recombinants in two different patients from Cameroon [72, 97]. M/O mosaic viruses can replicate well in vivo and in vitro, and can even become the predominant variant within the patient's viral population . Recombination between such divergent strains could contribute substantially to the emergence of new HIV-1 variants, and would have important implications both for diagnosis by serological and molecular tests, and for treatment.
The phylogenetic position of YBF-30 and YBF-106, the only two group N representatives for which full genome sequences are so far available, depends of the gene studied. Using sequences from the 5 half of the genome, group N forms an independent lineage most closely related to, but still distant from, group M. In contrast, with sequences from the 3 half of the genome, group N viruses cluster more closely with a chimpanzee virus (SIVcpzUS) [17, 25]. These data suggest that group N viruses are the result of a recombination event between an SIVcpz like and an HIV-1 like virus. This observation offers further substantiation of a chimpanzee-human zoonosis.
These observations also open the hypothesis that distant SIVs and
HIVs can potentially recombine, particularly in individuals who are
exposed to SIV by cross-species transmission. By this means novel SIV
sequences may be introduced more efficiently into the human
Figure 4. Evolutionary relationships of the Circulating Recombinant Forms, CRF01-AE, CRF02-AG, CRF06-cpx and CRF11-cpx in different regions of the genome, based on neighbor joining phylogenetic trees of partial gag sequences (p24) and partial env sequences (V3-V5).
While dual infections with HIV-1 and HIV-2 have frequently been reported in regions where both viruses circulate , as yet no recombinants between them have been described. In this case, the level of genetic divergence may be too high for successful recombination, although its possibility cannot be entirely excluded.
Methods to identify recombinants
Recombinants can only be detected if different parts of the genome are genetically characterized, either by sequencing or by more simplified subtyping techniques such as HMA in env and gag [19, 30]. Nevertheless, sequencing remains the most accurate approach to identify HIV-1 variants, especially recombinants or CRFs. Even only partial gag and/or env sequences give more precise information than HMA with regard to the presence of subclades or recombinant viruses (Figure 4). CRFs can form subclusters within a certain subtype. For example in phylogenetic trees, CRF02-AG strains form a different subcluster among subtype A in env and gag, whereas env HMA cannot discriminate CRF02-AG strains from subtype A. Also, CRF06-cpx strains form a separate subcluster within subtype G in the envelope, and a separate subcluster within subtype A in the gag region. Subtype A sequences from the CRF01-AE strains, form also a separate subcluster, see Figure 4.
Only full-length sequencing can determine the exact pattern of mosaicism within an isolate that is recombinant. A variety of complementary approaches have been developed to identify sequences that are recombinants, and to map the positions of breakpoints within mosaic sequences. Because the different subtypes of HIV-1 have been well defined, potential intersubtype recombinants can be analyzed in a more-or-less automated fashion. Using moving window analysis, diversity or similarity plots [23, 50] can be used to display the extent of difference or similarity of a new sequence to representatives of other subtypes. The Recombinant Identification Program (RIP)  uses distance measures to assign subtypes to regions within the new sequence. Bootscanning assesses the strength of bootstrap support for the phylogenetic placement of the new sequence with any subtype representative. For bootscanning, neighbor joining trees for windows moving along the alignment are done and the bootstrap values for the studied sequences are plotted at the midpoint of each window resulting in bootstrap plots . Fine-scale mapping of recombination breakpoints has been performed using informative site analysis [23, 81]. Much of the software used to perform these analyses is freely available from the authors, or can be accessed on-line. Summaries of and links to the different programs are available on the Los Alamos HIV Database website (http://hiv-web.lanl.gov/) and David Robertson's site at http://grinch.zoo.ox.ac.uk/RAPlinks.html.
Worldwide distribution of HIV-1 variants
Subtype designations have been powerful molecular epidemiological markers to track the course of the HIV-1 pandemic. It seems clear that the various subtypes, subclades within subtypes, and CRFs have been generated by epidemiological accidents. Figure 5 shows the geographic distribution of HIV-1 subtypes and CRFs.The predominant viral forms in the global epidemic are subtypes A and C, followed by subtype B and the recombinants CRF01-AE and CRF02-AG [57, 74, 110]. The greatest genetic diversity of HIV-1 has been found in Africa , especially Central Africa. Overall subtypes A and C and CRF02-AG are most common, but all groups and subtypes are found, consistent with this continent being the source of the epidemic . In South and East Africa subtype C predominates [31, 36, 104]. In West and West Central Africa, the majority of viruses are CRF02-AG . In North America, Europe and Australia, subtype B is by far the most common. However, various other group M subtypes, and even group O viruses, have been reported in the US [5, 10, 11, 78, 109] and several European countries [1, 30, 46, 90] and there the unusual subtypes even seem to be increasing [8, 20, 92]. In South America, subtype B predominates, but subtypes F and C are also found [38, 54, 84]. Different subtypes circulate in Asia, subtype C predominates in India and CRF01-AE is predominant in southeast Asia.
The exact prevalence of recombinant strains is not well known,
since few systematic studies have been conducted to address this
problem. Preliminary data show that for example in Africa, the
Figure 5. Geographic distribution of HIV-1 subtypes and CRFs.
proportions of discordant gag/env samples can vary from less than 10% to up to 40% according to the countries or regions studied [56, 61, 73, 79, 80, 98, 105]. The subtypes involved in these discordant samples, depend on the subtypes that co-circulate in a certain region, for instance, in Nigeria only subtypes A and G co-circulate and are the only subtypes involved in the 37 discordant samples [56, 73]. As expected, given the presence of numerous co-circulating subtypes, a wide variety of recombinants has been reported in DRC and all subtypes are involved in the 29 discordant samples .
The global distribution of different forms of HIV-1 is a dynamic process. As more HIV-1 variants inevitably intermix in different parts of the world the likelihood of generating new recombinant viruses will increase. The pattern of mosaicism will become even more complex, since recombination involving viruses that are already recombinant will occur. Mosaics involving CFR02AG have already been observed in various African countries [39, 61, 72]. Continued monitoring is necessary to determine the future role of non-subtype B viruses in North America and Europe, and to chart the emergence of new predominant subtypes and CRFs around the world.
Implications of recombination
Recombinant viruses may have some advantages over the parental strain, including eventual modifications in tropism and replication efficiency (fitness). Several studies have found that, under the selective pressure imposed by antiretroviral drugs, recombination between strains with different drug sensitivities occurred, resulting in new HIV-1 variants with dual drug resistance . In vitro experiments with feline and murine retroviruses have demonstrated that mixed infections can generate recombinant viruses with altered tissue tropism, pathogenicity, and host range, or with changes in antigenic epitopes [27, 102]. Finally, recombination also has important implications for vaccine strategies based on live-attenuated viruses, since these could recombine with infecting strains, even if the two are quite divergent.
The discovery of large numbers of recombinant viruses clearly
implies that coinfection with divergent HIV-1 strains is not as rare
as once thought. Indeed, dual infections with different subtypes have
been reported in regions where multiple variants co-circulate [6,
38, 72, 77, 96, 114]. It remains to be determined when
superinfection can occur during the course of HIV infection. In
macaques, it has recently been shown that superinfection with
divergent strains of HIV-2 is possible only during certain
periods when antibodies are not yet efficiently expressed . In contrast, in a chimpanzee, superinfection with a CRF01-AE virus 32 weeks after experimental infection with a subtype B strain led to a dual infection with the rapid appearance of recombinant viruses . The latter result suggests that superinfection is not restricted to the early phase of infection, and implies that the humoral and cellular immune response are not efficient against divergent strains.
Conclusions and perspectives
The geographical distribution of subtypes is a dynamic and unpredictable process and intermixing of HIV-1 variants is inevitable. Recombinant viruses contribute already substantially to the global pandemic, and the likelihood of generating recombinant viruses will only continue to increase as the different HIV-1 subtypes spread to all continents, and even recombinant viruses will recombine. The proportion of recombinant viruses will depend on the prevalence rates of different subtypes, the probability that certain population groups acquire multiple infections and transmit their viruses further, and the fitness of any mosaic viruses generated. However, the frequency of recombinant viruses is almost certain to increase; recombination, once it has occurred, cannot be undone. In future molecular epidemiologic studies, pure subtypes and CRFs have to be monitored. More studies are needed to understand the role and the implications of recombinant viruses in the global HIV evolution. It is important to study in more detail the impact of viral recombination on viral properties, since recombination may introduce genetic and biological consequences that are far greater than those resulting from the steady accumulation of single mutations. In order to develop an efficient vaccine, it remains to be determined when superinfection can occur during the course of HIV infection, and to what extend humoral and cellular immune response are efficient against divergent strains.
 Alaeus A, Leitner T, Lidman K, Albert J. Most HIV-1 genetic subtypes have entered Sweden. AIDS 1997, 11:199-202.
 Alizon M, Wain-Hobson S, Montagnier L, Sonigo P. Genetic variability of the AIDS virus: nucleotide sequence analysis of two isolates from African patients. Cell 1986, 46:63-74.
 Anderson Jon P., Allen G. Rodrigo, Gerald H. Learn, Anup Madan, Claire Delahunty, Michael Coon, Marc Girard, Saladin Osmanov, Leroy Hood, and James I. Mullins Testing the Hypothesis of a Recombinant Origin of Human Immunodeficiency Virus Type 1 subtype E, J Virol 2000, 74:10752-10765.
 Andersson S, Norrgren H, Dias F, Biberfeld G, Albert J. Molecular characterization of human immunodeficiency virus (HIV)-1 and -2 in individuals from Guinea-Bissau with single or dual infections: predominance of a distinct HIV-1 subtype A/G recombinant in West Africa. Virology 1999, 262:312-320.
 Artenstein AW, Coppola J, Brown AE, Carr JK, Sanders-Buell E, Galbarini E, Mascola JR, VanCott TC, Schonbrood P, McCutchan FE. Multiple introductions of HIV-1 subtype E into the western hemisphere. Lancet 1995, 346:1197-1198.
 Artenstein AW, VanCott TC, Mascola JR, Carr JK, Hegerich PA, Gaywee J, Sanders-Buell E, RobbML, Dayhoff DE, Thitivichianlert S. Dual infection with human immunodeficiency virus type 1 of distinct envelope subtypes in humans. J Infect Dis 1995, 171:805-810.
 Ayouba A, Souquieres S, Njinku B, Martin PM, Muller-Trutwin MC, Roques P, Barre-Sinoussi F, Mauclere P, Simon F, Nerrienet E. HIV-1 group N among HIV-1-seropositive individuals in Cameroon. AIDS 2000, 14:2623-2625.
 Barin F, Courouce AM, Pillonel J, Buzelay L. The retrovirus study group of the French society of blood transfusion: Increasing diversity of HIV-1M serotypes in French blood donors over a 10-year period (1985-1995). AIDS 1997, 11:1503-1508.
 Bobkov A, Kazennova E, Selimova L, Bobkova M, Khanina T, Ladnaya N, Kravchenko A, Pokrovsky V, Cheingsong-Popov R, Weber J. A sudden epidemic of HIV type 1 among injecting drug users in the former Soviet Union: identification of subtype A, subtype B, and novel gagA/envB recombinants. AIDS Res Hum Retroviruses 1998, 14:669-676.
 Brodine SK, Mascola JR, Weiss PJ, Ito SI, Porter KR, Artenstein AW, Garland FC, McCutchan FE, Burke DS. Detection of diverse HIV-1 genetic subtypes in the United States. Lancet 1995, 346:1198-1199.
 Brodine SK, Shaffer RA, Starkey MJ, Tasker SA, Gilcrest JL, Louder MK, Barile A, VanCott TC, Vahey MT, McCutchan FE, Birx DL, Richman DD, Mascola JR. Drug resistance patterns, genetic subtypes, clinical features, and risk factors in military personnel with HIV-1 seroconversion. Ann intern Med 1999, 131:502-506.
 Carr JK, Salminen MO, Koch C, Gotte D, Artenstein AW, Hegerich PA, St Louis D, Burke DS, McCutchan FE. Full-length sequence and mosaic structure of a human immunodeficiency virus type 1 isolate from Thailand. J Virol 1996, 70:5935-5943.
 Carr JK, Salminen MO, Albert J, Sanders-Buell E, Gotte D, Birx DL, McCutchan FE. Full genome sequences of human immunodeficiency virus type 1 subtypes G and A/G intersubtype recombinants. Virology. 1998, 247:22-31.
 Carr JK, Laukkanen T, Salminen MO, Albert J, Alaeus A, Kim B, Sanders-Buell E, Birx DL, McCutchan FE. Characterization of subtype A HIV-1 from Africa by full genome sequencing. AIDS. 1999, 13:1819-1826.
 Carr JK, Foley B, Leitner T, Salminen M, Korber BT, McCutchan FE. Reference sequences representing the principal genetic diversity of HIV-1 in the pandemic. In : Human Retrovirus and AIDS. Edited by Los Alamos National Laboratory, Los Alamos NM, 1998 Part III.
 Choi DJ, Dube S, Spicer TP, Slade HB, Jensen FC, Poiesz BJ. HIV type 1 isolate Z321, the strain used to make a therapeutic HIV type 1 immunogen, is intersubtype recombinant. AIDS Res Hum Retroviruses 1997, 13:357-361.
 Corbet S, Muller-Trutwin MC, Versmisse P, Delarue S, Ayouba A, Lewis J, Brunak S, MartinP, Brun-Vezinet F, Simon F, Barre-Sinoussi F, Mauclere P. Env sequences of simian immunodeficiency viruses from chimpanzees in Cameroon are strongly related to those of human immunodeficiency virus group N from the same geographic area. J Virol 2000, 74:529-534.
 Cornelissen M, Van Den Burg R, Zorgdrager F, Goudsmit J. Spread of distinct human immunodeficiency virus type 1 AG recombinant lineages in Africa. J Gen Virol 2000, 81:363-374.
 Delwart EL, Shpaer EG, Louwagie J, McCutchan FE, Grez M, Rubsamen-Waigmann H, Mullins JI. Genetic relationships determined by a DNA heteroduplex mobility assay: analysis of HIV-1 env genes. Science 1993, 262:1257-1261.
 Dietrich U, Ruppach H, Gehring S, Knechten H, Knickmann M, Jager H, Wolf E, Husak R, Orfanos CE, Brede HD, Rubsamen-Waigmann H, von Briesen H. Large proportion of non-B HIV-1 subtypes and presence of zidovudine resistance mutations among German seroconverters. AIDS 1997, 11:1532-1533.
 Fultz P, Yue L, Wei Q, Girard M. Human immunodeficiency virus type 1 intersubtype (B/E) recombination in a superinfected chimpanzee. J Virol 1997, 71:7990-7995.
 Gao F, Robertson DL, Morrison SG, Hui H, Craig S, Decker J, Fultz PN, Girard M, Shaw GM, Hahn BH, Sharp PM. The heterosexual human immunodeficiency virus type 1 epidemic in Thailand is caused by an intersubtype (A/E) recombinant of African origin. J Virol 1996, 70:7013-7029.
 Gao F, Robertson DL, Carruthers CD, Morrison SG, Jian B, Chen Y, Barre-Sinoussi F, Girard M, Srinivasan A, Abimiku AG, Shaw GM, Sharp PM, Hahn BH. A comprehensive panel of near-full-length clones and reference sequences for non-subtype B isolates of human immunodeficiency virus type. J Virol 1998, 72:5680-5698.
 Gao F, Robertson DL, Carruthers CD, Li Y, Bailes E, Kostrikis LG, Salminen MO, Bibollet-Ruche F, Peeters M, Ho DD, Shaw GM, Sharp PM, Hahn BH. An isolate of human immunodeficiency virus type 1 originally classified as subtype I represents a complex comprising three different group M subtypes (A, G, and I). J Virol 1998, 72:10234-10241.
 Gao F, Bailes E, Robertson DL, Chen Y, Rodenburg CM, Michael SF, Cummins LB, Arthur LO, Peeters M, Shaw GM, Sharp PM, Hahn BH. Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes. Nature 1999, 397:436-441.
 Gao F, Vidal N, Li Y, Trask S, Chen Y, Kostrikis L, Ho D, Oh M, Salminen M, Robertson D, ShawG, Hahn B, Peeters M. Evidence for Two Distinct Sub-subtypes within the HIV-1 subtype A Radiation. AIDS Res Hum Retroviruses (submitted).
 Golovkina T, Jaffe A, Ross S. Coexpression of exogenous and endogenous mouse mammary tumor viruses RNA in vivo results in viral recombination and broadens the virus host range. J Virol 1994, 68:5019-5026.
 Goodrich DW, Duesberg PH ; Retroviral recombination during reverse transcription. Proc Natl Acad Sci USA 1990, 87: 2050-2056.
 Graf M, Shao Y, Zhao Q, Seidl T, Kostler J, Wolf H, Wagner R. Cloning and characterization of a virtually full-length HIV type 1 genome from a subtype B-Thai strain representing the most prevalent B-clade isolate in China. AIDS Res Hum Retroviruses. 1998, 14:285-288.
 Heyndrickx L, Janssens W, Coppens S, Vereecken K, Willems B, Fransen K, Colebunders R, Vandenbruaene M, van der Groen G. HIV type 1 C2V3 env diversity among Belgian individuals. AIDS Res Hum Retroviruses 1998, 14: 1291-1296.
 Heyndrickx L, Janssens W, Zekeng L, Musonda R, Anagonou S, Van der Auwera G, Coppens S, Vereecken K, De Witte K, Van Rampelbergh R, Kahindo M, Morison L, McCutchan FE, CarrJK, Albert J, Essex M, Goudsmit J, Asjo B, Salminen M, Buve A, van Der Groen G. Simplified strategy for detection of recombinant human immunodeficiency virus type 1 group M isolates by gag/env heteroduplex mobility assay. Study Group on Heterogeneity of HIV Epidemics in African Cities. J Virol 2000, 74:363-370.
 Ho DD, Neumann AU, Perelson AS, Chen W, Leonard JM, Markowitz M. Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. Nature 1995, 373:123-6.
 Hoelscher M, Hanker S, Barin F, Cheingsong-Popov R, Dietrich U, Jordan-Harder B, Olaleye D, Nagele E, Markuzzi A, Mwakagile D, Minja F, Weber J, Gurtler L, Von Sonnenburg F.. HIV-1 V3 serotyping in Tanzanian samples: possible reasons for mismatching with genetic subtyping. AIDS Res Hum Retroviruses 1998, 14:139-149.
 Howard TM, Rasheed S. Genomic structure and nucleotide sequence analysis of a new HIV type 1 subtype A strain from Nigeria. AIDS Res Hum Retroviruses 1996, 12:1413-1425.
 Hu WS, Temin HM. Retroviral recombination and reverse transcription. Science 1990, 250:1227-1233.
 Hussein M, Abebe A, Pollakis G, Brouwer M, Petros B, Fontanet AL, de Wit TF. HIV-1 subtype C in commercial sex workers in Addis Ababa, Ethiopia. J Acquir Immune Defic Syndr. 2000, 23:120-127.
 Jameel S, Zafrullah M, Ahmad M, Kapoor GS, Sehgal SA. Genetic analysis of HIV-1 from Punjab, India reveals the presence of multiple variants. AIDS 1995, 9:685-690.
 Janini LM, Tanuri A, Schechter M, Peralta JM, Vicente AC, Dela Torre N, Pieniazek NJ, Luo CC, Ramos A, Soriano V, Schochetman G, Rayfield MA, Pieniazek D. Horizontal and vertical transmission of human immunodeficiency virus type 1 dual infections caused by viruses of subtypes B and C. J Infect Dis 1998, 177:227-231.
 Janssens W, Salminen MO, Laukkanen T, Heyndrickx L, van der Auwera, Colebunders R, McCutchan FE, van der Groen G. Near full-length genome analysis of HIV type 1 CRF02. AG subtype C and CRF02. AG subtype G recombinants. AIDS Res Hum Retroviruses 2000, 16:1183-1189.
 Jonassen TO, Grinde B, Asjo B, Hasle G, Hungnes O. Intersubtype recombinant HIV type 1 involving HIV-MAL-like and subtype H-like sequence in four Norwegian cases. AIDS Res Hum Retroviruses 2000, 16:49-58.
 Kanki PJ, Peeters M, Gueye-Ndiaye A. Virology of HIV-1 and HIV-2: implications for Africa. AIDS 1997, 11 Suppl B: S33-S42.
 Kato K, Shiino T, Kusagawa S, Sato H, Nohtomi K, Shibamura K, Nguyen TH, Pham KC, Truong XL, Mai HA, Hoang TL, Bunyaraksyotin G, Fukushima Y, Honda M, Wasi C, Yamazaki S, Nagai Y, Takebe Y. Genetic similarity of HIV type 1 subtype E in a recent outbreak among injecting drug users in northern Vietnam to strains in Guangxi Province of southern China. AIDS Res Hum Retroviruses 1999, 15:1157-1168.
 Kostrikis L, Bagdades E, Cao Y, Zhang L, Dimitriou D, Ho D. Genetic analysis of human immunodeficiency virus type 1 strains from patients in Cyprus: identification of a new subtype designated subtype I. J Virol 1995, 69:6122-6130.
 Koulinska I, Ndung T, Mwakagile D, Msamanga G, Kagoma C, Fawzi W, Essex M, Renifjo B. A new human immunodeficiency virus type 1 circulating recombinant form from Tanzania. AIDS Res Hum Retroviruses, 2001, in press.
 Kuiken CL, Foley B, Hahn B, Korber B, McCutchan F, Marx PA, Mellors JW, Mullins JI, Sodroski J, and Wolinsky S, Eds. Human Retroviruses and AIDS 1999: A Compilation and Analysis of Nucleic Acid and Amino Acid Sequences. Theoretical Biology and Biophysics Group, Los Alamos National Laboratory, Los Alamos, NM.
 Lasky M, Perret JL, Peeters M, Bibollet-Ruche F, Liegeois F, Patrel D, Molinier S, Gras C, Delaporte E. Presence of non-B subtypes and divergent subtypes B strains of HIV-1 in individuals infected after overseas deployment. AIDS 1997,11:43-51.
 Laukkanen T, Carr JK, Janssens W, Liitsola K, Gotte D, McCutchan FE, Op de Coul E, Cornelissen M, Heyndrickx L, van der Groen G, Salminen MO. Virtually full-length subtype F and F/D recombinant HIV-1 from Africa and South America. Virology 2000, 269:95-104.
 Liitsola K, Tashkinova I, Laukkanen T, Korovina G, Smolskaja T, Momot O, Mashkilleyson N, Chaplinskas S, Brummer-Korvenkontio H, Vanhatalo J, Leinikki P, Salminen MO. HIV-1 genetic subtype A/B recombinant strain causing an explosive epidemic in injecting drug users in Kaliningrad. AIDS 1998, 12:1907-1919.
 Liitsola K, Holm K, Bobkov A, Pokrovsky V, Smolskaya T, Leinikki P, Osmanov S, Salminen M. An AB recombinant and its parental HIV type 1 strains in the area of the former Soviet Union: low requirements for sequence identity in recombination. UNAIDS Virus Isolation Network. AIDS Res Hum Retroviruses 2000, 16:1047-1053.
 Lole KS, Bollinger RC, Paranjape RS, Gadkari D, Kulkarni SS, Novak NG, Ingersoll R, Sheppard HW, Ray SC. Full-length human immunodeficiency virus type 1 genomes from subtype C infected seroconverters in India, with evidence of intersubtype recombination. J Virol 1999, 73:142-160.
 Louwagie J, McCutchan FE, Peeters M, Brennan TP, Sanders-Buell E, Eddy GA, van der Groen G, Fransen K, Gershy-Damet GM, Deleys R, et al. Phylogenetic analysis of gag genes from 70 international HIV-1 isolates provides evidence for multiple genotypes. AIDS 1993, 7:769-780.
 Louwagie J, Janssens W, Mascola J, Heyndrickx L, Hegerich P, van der Groen G, McCutchan FE, Burke DS. Genetic diversity of the envelope glycoprotein from human immunodeficiency virus type 1 isolates of African origin. J Virol 1995, 69:263-271.
 Luo CC, Tian C, Hu DJ, Kai M, Dondero T, Zheng X. HIV-1 subtype C in China. Lancet 1995, 345:1051-1052
 Marquina S, Leitner T, Rabinovich RD, Benetucci J, Libonatti O, Albert J. Coexistence of subtypes B, F, and as B/F env recombinant of HIV type 1 in Buenos Aires Argentina. AIDS Res Hum Retroviruses 1996, 12:1651-1654.
 Mauclere P, Loussert-Ajaka I, Damond F, Fagot P, Souquieres S, Monny Lobe M, Mbopi Keou FX, Barre-Sinoussi Saragosti S, Brun-Vezinet F, Simon F. Serological and virological characterization of HIV-1 group O infection in Cameroon. AIDS. 1997, 11:445-453.
 McCutchan FE, Carr JK, Bajani M, Sanders-Buell E, Harry TO, Stoeckli TC, Robbins KE, Gashau W, Nasidi A, Janssens W, Kalish ML. Subtype G and multiple forms of A/G intersubtype recombinant human immunodeficiency virus type 1 in Nigeria. Virology. 1999, 254:226-234.
 McCutchan F. Understanding the genetic diversity of HIV. AIDS 2000, 14 (suppl), S31-S44.
 Menu E, Truong TX, Lafon ME, Nguyen TH, Muller-Trutwin MC, Nguyen TT, Deslandres A, Chaouat G, Duong QT, Ha BK, Fleury HJ, Barre-Sinoussi F. HIV type 1 Thai subtype E is predominant in South Vietnam. AIDS Res Hum Retroviruses 1996, 12:629-633.
 Menu E, Reynes JM, Muller-Trutwin MC, Guillemot L, Versmisse P, Chiron M, An S, Trouplin V, Charneau P, Fleury H, Barre-Sinoussi F, Sainte Marie FF. Predominance of CCR5-dependent HIV-1 subtype E isolates in Cambodia. J Acquir Immune Defic Syndr Hum Retrovirol 1999, 20:481-487.
 Montavon C, Bibollet-Ruche F, Robertson D, Koumare B, Mulanga C, Esu-Williams E, Toure C, Mboup S, Saman E, Delaporte E, Peeters M. The identification of a complex A/G/I/J recombinant HIV type 1 virus in various West African countries. AIDS Res Hum Retroviruses 1999, 15:1707-1712.
 Montavon C, Toure-Kane C, Liegeois F, Mpoudi E, Bourgeois A, Vergne L, Perret JL, Boumah A, Saman E, Mboup S, Delaporte E, Peeters M. Most env and gag subtype A HIV-1 viruses circulating in West and West Central Africa are similar to the prototype AGrecombinant virus IBNG. J Acquir Immune Defic Syndr 2000, 23:363-374.
 Motomura K, Kusagawa S, Kato K, Nohtomi K, Lwin HH, Tun KM, Thwe M, Oo KY, Lwin S, Kyaw O, Zaw M, Nagai Y, Takebe Y. Emergence of new forms of human immunodeficiency virus type 1 intersubtype recombinants in Central Myanmar. AIDS Res Human Retroviruses 2000, 17:1831-1843.
 Moutouh L, Corbeil J, Richman D. Recombination leads to the rapid emergence of HIV-1 dually resistant mutants under selective drug pressure. Proc Natl Acad Sci USA 1996, 93:6106-6111
 Muller-Trutwin MC, Chaix ML, Letourneur F, Begaud E, Beaumont D, Deslandres A, You B, Morvan J, Mathiot C, Barre-Sinoussi F, Saragosti S. Increase of HIV-1 subtype A in Central African Republic. J Acquir Immune Defic Syndr 1999, 21:164-171.
 Nasioulas G, Paraskevis D, Magiorkinis E, Theodoridou M, Hatzakis A. Molecular analysis of the full-length genome of HIV-1 subtype I: evidence of A/G/I recombination. AIDS Res Hum Retroviruses 1999, 15:745-758.
 Nkengasong JN, Janssens W, Heyndrickx L, Fransen K, Ndumbe PM, Motte J, Leonaers A, Ngolle M, Ayuk J, Piot P, et al. Genotypic subtypes of HIV-1 in Cameroon. AIDS. 1994, 8:1405-1412.
 Nkengasong JN, Luo CC, Abouya L, Pieniazek D, Maurice C, Sassan-Morokro M, Ellenberger D, Hu DJ, Pau CP, Dobbs T, Respess R, Coulibaly D, Coulibaly IM, Wiktor SZ, Greenberg AE, Rayfield M. Distribution of HIV-1 subtypes among HIV-seropositive patients in the interior of Cote d`Ivoire. J Acquir Immune Defic Syndr. 2000, 23:430-436.
 Oelrichs RB, Workman C, Laukkanen T, McCutchan FE, and Deacon NJ: A novel subtype recombinant full-length HIV type 1 genome from Burkina Faso. AIDS Res Hum Retroviruses 1998, 14:1495-1500.
 Otten RA, Ellenberger DL, Adams DR, Fridlund CA, Jackson E, Pieniazek D, Rayfield MA.. Identification of a window period for susceptibility to dual infection with two distinct Human Immunodeficiency virus type 2 isolates in a Macaca nemestrina (Pig-tailed Macaque) model. J Infec Diseases 1999, 180:673-684.
 Paraskevis D, Magiorkinis M, Paparizos V, Pavlakis GN, Hatzakis A. Molecular characterization of a recombinant HIV type 1 isolate (A/G/E/?): unidentified regions may be derived from parental subtype E sequences. AIDS Res Hum Retroviruses 2000, 16:845-855.
 Peeters M, Gueye A, Mboup S, Bibollet-Ruche F, Ekaza E, Mulanga C, Ouedrago R, Gandji T, Mpele P, Dibanga G, Koumare B, Saidou M, Esu-Williams E, Lombart J, Badombena W, Nkandu L, Vanden Haesevelde M, Delaporte E. Geographic distribution of HIV-1 group O viruses in Africa. AIDS 1997, 11:493-498.
 Peeters M, Liegeois F, Torimiro N, Bourgeois A, Mpoudi E, Vergne L, Saman E, Delaporte E, Saragosti S. Characterization of a highly replicative intergroup M/O recombinant HIV-1 virus isolated from a Cameroonian patient. J Virol 1999, 73:7368-7375
 Peeters M, Esu-Williams E, Vergne L, Montavon C, Mulanga-Kabeya C, Harry T, Ibironke A, Lesage D, Patrel D, Delaporte E. Predominance of subtype A and G HIV type 1 in Nigeria, with geographical differences in their distribution. AIDS Res Hum Retroviruses. 2000, 16(4):315-25.
 Peeters M, Sharp P . The genetic diversity of HIV-1 : the moving target. AIDS 2000, 14 suppl 3:s129-140
 Piyasirisilp S, McCutchan FE, Carr JK, Sanders-Buell E, Liu W, Chen J, Wagner R, Wolf H, Shao Y, Lai S, Beyrer C, YuXF. A Recent Outbreak of Human Immunodeficiency Virus Type 1 Infection in Southern China Was Initiated by Two Homogeneous, Geographically Separated Strains, Circulating Recombinant Form AE and a Novel BC. J Virol 2000, 74:11286-11295.
 Preston BD, Poiesz BJ, Loeb LA. Fidelity of HIV-1 reverse transcriptase. Science 1988, 242 :1168-1171
 Quinones-Mateu M, Arts EJ. Recombination in HIV-1: update and implications. AIDS Rev 1999, 1:89-100.
 Rayfield MA, Sullivan P, Bandea CI, Britvan L, Otten RA, Pau CP, Pieniazek D, Subbarao S, Simon P, Schable CA, Wright AC, Ward J, Schochetman G. HIV-1 group O virus identified for the first time in the United States. Emerg Infect Dis 1996, 2:209-212.
 Renjifo B, Chaplin B, Mwakagile D, Shah P, Vannberg F, Msamanga G, Hunter D, Fawzi W, Essex M. Epidemic expansion of HIV type 1 subtype C and recombinant genotypes in Tanzania. AIDS Res Hum Retroviruses. 1998, 14:635-638.
 Renjifo B, Gilbert P, Chaplin B, Vannberg F, Mwakagile D, Msamanga G, Hunter D, Fawzi W, Essex M. Emerging recombinant human immunodeficiency viruses: uneven representation of the envelope V3 region. AIDS 1999, 13:1613-1621.
 Robertson DL, Hahn BH, Sharp PM. Recombination in AIDS viruses. J Mol Evol. 1995, 40:249-259
 Robertson DL, Anderson JP, Bradac JA, Carr JK, Foley B, Funkhouser RK, Gao F, Hahn BH, Kalish ML, Kuiken C, Learn GH, Leitner T, McCutchan F, Osmanov S, Peeters M, Pieniazek D, Salminen M, Sharp PM, Wolinsky S, Korber B. HIV-1 nomenclature proposal. Science. 2000, 288:55-56.
 Robertson DL, Anderson JP, Bradac JA, Carr JK, Foley B, Funkhouser RK, Gao F, Hahn BH, Kalish ML, Kuiken C, Learn GH, Leitner T, McCutchan F, Osmanov S, Peeters M, Pieniazek D, Salminen M, Sharp PM, Wolinsky S, Korber B. HIV-1 nomenclature proposal. Human Retroviruses and AIDS 1999: A Compilation and Analysis of Nucleic Acid and Amino Acid Sequences. Kuiken CL, Foley B, Hahn B, Korber B, McCutchan F, Marx PA, Mellors JW, Mullins JI, Sodroski J, and Wolinksy S, Eds. Theoretical Biology and Biophysics Group, Los Alamos National Laboratory, Los Alamos, NM.
 Russell KL, Carcamo C, Watts DM, Sanchez J, Gotuzzo E, Euler A, Blanco JC, Galeano A, Alava A, Mullins JI, Holmes KK,Carr JK. Emerging genetic diversity of HIV-1 in South America. AIDS 2000, 14:1785-1791.
 Sabino EC, Shpaer EG, Morgado MG, Korber BT, Diaz RS, Bongertz V, Cavalcante S, Galvao-Castro B, Mullins JI, Mayer A. Identification of human immunodeficiency virus type 1 envelope genes recombinant between subtypes B and F in two epidemiologically linked individuals from Brazil. J Virol 1994, 68:6340-6346.
 Salminen MO, Carr JK, Burke DS, McCutchan FE. Identification of breakpoints in intergenotypic recombinants of HIV type 1 by bootscanning. AIDS Res Hum Retroviruses. 1995, 11:1423-1425.
 Salminen MO, Carr JK, Robertson DL, Hegerich P, Gotte D, Koch C, Sanders-Buell E, Gao F, Sharp PM, Hahn BH, Burke DS, McCutchan FE. Evolution and probable transmission of intersubtype recombinant human immunodeficiency virus type 1 in a Zambian couple. J Virol 1997, 71:2647-2655.
 Salminen M, Gao F, Janssens W, McCutchan F. The loss of HIV-1 subtype I. XIII International Conference on AIDS. Durban 2000, A2065
 Siepel AC, Halpern AL, Macken C, Korber BT. A computer program designed to screen rapidly for HIV type 1 intersubtype recombinant sequences. AIDS Res Hum Retroviruses 1995, 11:1413-1416.
 Simon F, Loussert-Ajaka I, Damond F, Saragosti S, Barin F, and Brun-Vzinet F: HIV type 1 diversity in northern Paris, France. AIDS Res Hum Retroviruses 1996;12:1427-1233.
 Simon F, Mauclere P, Roques P, Loussert-Ajaka I, Muller-Trutwin MC, Saragosti S, Georges-Courbot MC, Barre-Sinoussi F, Brun-Vezinet F. Identification of a new human immunodeficiency virus type 1 distinct from group M and group O. Nat Med. 1998, 4:1032-1037.
 Sonnerborg A, Durdevic S, Giesecke J, Sallberg M. Dynamics of the HIV-1 subtype distribution in the Swedish HIV-1 epidemic during the period 1980-1993. AIDS Res Human Retroviruses 1997, 13:343-345.
 Srinivasan A, York D, Butler D Jr, Jannoun-Nasr R, Getchell J, McCormick J, Ou CY, Myers G, Smith T, Chen E. Molecular characterization of HIV-1 isolated from a serum collected in 1976: nucleotide sequence comparison to recent isolates and generation of hybrid HIV. AIDS Res Hum Retroviruses 1989, 5:121-129.
 Stuhlmann H, Berg P. Homologous recombination of copackaged retrovirus RNAs during reverse transcription. J Virol 1992, 66:2378-2388 ;
 Su L, Marcus Graf, Yuanzhi Zhang, Hagen von Briesen, Hui Xing, Josef Kstler, Holger Melzl, Hans Wolf, Yiming Shao, and Ralf Wagner Characterization of a Virtually Full-Length Human Immunodeficiency Virus Type 1 Genome of a Prevalent Intersubtype (C/B) Recombinant Strain in China. J Virol 2000 74:11367-11376.
 Takehisa J, Zekeng L, Miura T, Ido E, Yamashita M, Mboudjeka I, Gurtler LG, Hayami M, Kaptue L. Triple HIV-1 infection with group O and Group M of different clades in a single Cameroonian AIDS patient. J Acquir Immune Defic Syndr Hum Retrovirol 1997, 14:81-82.
 Takehisa J, Zekeng L, Ido E, Yamaguchi-Kabata Y, Mboudjeka I, Harada Y, Miura T, Kaptu L, Hayami M.. Human immunodeficiency virus type 1 intergroup (M/O) recombination in Cameroon. J Virol 1999, 73:6810-6820.
 Toure-Kane C, Montavon C, Faye MA, Gueye PM, Sow PS, Ndoye I, Gaye-Diallo A, Delaporte E, Peeters M, Mboup S. Identification of all HIV type 1 group M subtypes in Senegal, a country with low and stable seroprevalence. AIDS Res Hum Retroviruses. 2000, 16:603-609.
 Tovanabutra S, De Souza M, Brown A, Birx D, McCutchan F, Carr J. First identified AE/B intersubtype recombinant of HIV-1 is found in Thailand. XIII International Conference on AIDS. Durban 2000, C2382.
 Triques K, Bourgeois A, Vidal N, Mpoudi-Ngole E, Mulanga-Kabeya C, Nzilambi N, Torimiro N, Saman E, Delaporte E, Peeters M. Near-full-length genome sequencing of divergent African HIV type 1 subtype F viruses leads to the identification of a new HIV type 1 subtype designated K. AIDS Res Hum Retroviruses 2000, 16:139-151.
 Tscherning-Casper C, Dolcini G, Mauclere P, Fenyo EM, Barre-Sinoussi F, Albert J, Menu E. Evidence of the existence of a new circulating recombinant form of HIV type 1 subtype A/J in Cameroon. The European Network on the Study of In Utero Transmission of HIV-1. AIDS Res Hum Retroviruses 2000, 16:1313-1318.
 Tumas KM, Poszgay JM, Avidan N, Ksiazek SJ, Overmoyer B, Blank KJ, Prystowsky MB. Loss of antigenic epitopes as the result of env gene recombination in retrovirus-induced leukemia in immunocompetent mice. Virology 1993, 192(2):587-595.
 Vanden Haesevelde M, Decourt JL, De Leys RJ, Vanderborght B, van der Groen G, van Heuverswijn H, Saman E. Genomic cloning and complete sequence analysis of a highly divergent African human immunodeficiency virus isolate. J Virol 1994, 68:1586-1596.
 Van Harmelen JH, Van der Ryst E, Loubser AS, York D, Madurai S, Lyons S, Wood R, Williamson C. A predominantly HIV type 1 subtype C-restricted epidemic in South African urban populations. AIDS Res Hum Retroviruses 1999, 15:395-398.
 Vidal Nicole, Martine Peeters, Claire Mulanga-Kabeya, Nzila Nzilambi, David Robertson, Wantabala Ilunga, Hurogo Sema, Kazadi Tshimanga, Beni Bongo, and Eric Delaporte Unprecedented Degree of Human Immunodeficiency Virus Type 1 (HIV-1) Group M Genetic Diversity in the Democratic Republic of Congo Suggests that the HIV-1 Pandemic Originated in Central Africa. J Virol 2000, 74:10498-10507.
 Vidal N, Mulanga-Kabeya C, Nzila N, Delaporte E, Peeters M. The identification of a complex env subtype E HIV-1 virus from the Democratic Republic of Congo, recombinant with A, G, H, J, K and unknown subtypes. AIDS Res Human Retroviruses, 2000. 16:2059-2064
 Wei X, Ghosh SK, Taylor ME et al. Viral dynamics in human immunodeficiency virus type 1 infection. Nature 1995, 373 :117-122
 Weniger BC, Takebe Y, Ou C-Y, Yamazaki S. The molecular epidemiology of HIV in Asia. AIDS 1994, 8 (suppl), S13-S26.
 Womack C, Roth W, Newmann C, Rissing P, Lovell R, Haburchak D, Essex M, Bond VC. Identification of non-B human immunodeficiency virus type 1 subtypes in rural Georgia. Journal of Inf Dis, 2001, 183:138-142
 Workshop report from the European Commission and the Joint United Nations Programme on HIV/AIDS. HIV-1 subtypes: implications for epidemiology, pathogenicity, vaccines and diagnostics. AIDS 1997, 11:UNAIDS17-UNAIDS36.
 Yu, X.-F., J. Chen, Y. Shao, C. Beyrer, B. Liu, Z. Wang, W. Liu, J. Yang, S. Liang, R. P. Viscidi, J. Gu, G. Gurri-Glass, and S. Lai. 1999. Emerging HIV infections with distinct subtypes of HIV-1 infection among injection drug users from geographically separate locations in Guangxi China. J. AIDS 22:180-188.
 Yu, X. F., J. Chen, Y. Shao, C. Beyrer, and S. Lai. 1998. Two subtypes of HIV-1 among injection-drug users in southern China. Lancet 351:1250
 Zekeng L, Gurtler L, Afane Ze E, Sam-Abbenyi A, Mbouni-Essomba G, Mpoudi-Ngolle E, Monny-Lobe M, Tapka JB, Kaptue L. Prevalence of HIV-1 subtype O infection in Cameroon: preliminary results. AIDS 1994, 8:1626-1628.
 Zhu T, Wang N, Carr A, Wolinsky S, Ho DD. Evidence for coinfection by multiple strains of human immunodeficiency virus type 1 subtype B in an acute seroconverter. J Virol 1995, 69:1324-1327.