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Outer-membrane protein subtypes of Haemophilus influenzae type b and spread of disease in day-care centers.

Isolates of Haemophilus influenzae type b with a distinctive outer-membrane protein subtype, designated 1H, were responsible for 11 of 13 cases of invasive infection in children attending six day-care centers with secondary cases of disease, in comparison to three of 14 cases in children attending 10 centers with single cases and two centers with unrelated cases. The other 11 cases were caused by type b isolates of six different subtypes. The secondary attack rate in contacts younger than four years of age exposed to disease due to isolates of the 1H subtype was 16 per 1,000, compared with 1.6 per 1,000 after exposure to disease caused by subtypes other than 1H (P less than 0.008). Carriage rates were increased in day-care-center contacts exposed to patients with disease, and most of the carriers were colonized by isolates with subtypes homologous to those responsible for the respective index cases. Both 1H and non-1H strains were capable of colonizing contacts, but 1H strains may be more pathogenic than other subtypes.

Bacterial Proteins↗

Autoimmune and chronic inflammatory disorders and risk of non-Hodgkin lymphoma by subtype.

BACKGROUND: Some autoimmune and chronic inflammatory disorders are associated with increased risks of non-Hodgkin lymphoma (NHL). Because different NHL subtypes develop at different stages of lymphocyte differentiation, associations of autoimmune and inflammatory disorders with specific NHL subtypes could lead to a better understanding of lymphomagenic mechanisms. METHODS: In a population-based case-control study in Denmark and Sweden, 3055 NHL patients and 3187 matched control subjects were asked about their history of autoimmune and chronic inflammatory disorders, markers of severity, and treatment. Logistic regression with adjustment for study matching factors was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for NHL overall and for NHL subtypes. RESULTS: Risks of all NHL were increased in association with rheumatoid arthritis (OR = 1.5, 95% CI = 1.1 to 1.9), primary Sjögren syndrome (OR = 6.1, 95% CI = 1.4 to 27), systemic lupus erythematosus (OR = 4.6, 95% CI = 1.0 to 22), and celiac disease (OR = 2.1, 95% CI = 1.0 to 4.8). All of these conditions were also associated with diffuse large B-cell lymphoma, and some were associated with marginal zone, lymphoplasmacytic, or T-cell lymphoma. Ever use of nonsteroidal anti-inflammatory drugs, systemic corticosteroids, and selected immunosuppressants was associated with risk of NHL in rheumatoid arthritis patients but not in subjects without rheumatoid arthritis. Also, multivariable adjustment for treatment had little impact on risk estimates. Psoriasis, sarcoidosis, and inflammatory bowel disorders were not associated with increased risk of NHL overall or of any NHL subtype. CONCLUSIONS: Our results confirm the associations between certain autoimmune disorders and risk of NHL and suggest that the associations may not be general but rather mediated through specific NHL subtypes. These NHL subtypes develop during postantigen exposure stages of lymphocyte differentiation, consistent with a role of antigenic drive in autoimmunity-related lymphomagenesis.

Adult↗

Sequence complexity of histone H1 subtypes.

H1 subtypes are involved in chromatin higher-order structure and gene regulation. H1 has a characteristic three-domain structure. We studied the length variation of the available H1 subtypes and showed that the length of the N-terminal and C-terminal domains was more variable than that of the central domain. The N-terminal and C-terminal domains were of low sequence complexity both at the nucleotide and at the amino acid level, whereas the globular domain was of high complexity. In most subtypes, low complexity was due only to cryptic simplicity, which reflects the clustering of a number of short and often imperfect sequence motifs. However, a subset of subtypes from eubacteria, plants, and invertebrates contained tandem repeats of short amino acid motifs (four to 12 residues), which could amount to a large proportion of the terminal domains. In addition, some other subtypes, such as those of Drosophila and mammalian H1t, were only marginally simple. The coexistence of these three kinds of subtypes suggests that the terminal domains could have originated in the amplification of short sequence motifs, which would then have evolved by point mutation and further slippage.

Animals↗

Identification of duplicated fourth alpha2-adrenergic receptor subtype by cloning and mapping of five receptor genes in zebrafish.

The alpha(2)-adrenergic receptors (alpha(2)-ARs) belong to the large family of rhodopsinlike G-protein-coupled receptors that share a common structure of seven transmembrane (TM) alpha-helices. The aims of this study were (1) to determine the number of alpha(2)-AR genes in a teleost fish, the zebrafish (Danio rerio), (2) to study the gene duplication events that generated the alpha(2)-AR subtypes, and (3) to study changes in receptor structure that have occurred since the divergence of the mammalian and fish lineages. Here, we report the cloning and chromosomal mapping of fish orthologs for all three mammalian alpha(2)-ARs. In addition, we identified a fourth alpha(2)-AR subtype with two duplicates in zebrafish. Chromosomal mapping showed that the zebrafish alpha(2)-AR genes are located within conserved chromosomal segments, consistent with the origin of the four alpha(2)-AR subtypes by two rounds of chromosome or block duplication before the divergence of the ray fin fish and tetrapod lineages. Thus, the fourth subtype has apparently been present in the common ancestor of vertebrates but has been deleted or is yet to be identified in mammals. The overall percentage identity between the fish and mammalian orthologs is 53% to 67%, and in the TM regions 80% to 87%. These values are clearly lower than what is observed between mammalian orthologs. Still, all of the residues thought to be important for alpha(2)-adrenergic ligand binding are conserved across species and subtypes, and even the most divergent regions of the fish receptors show clear "molecular fingerprints" typical for orthologs of a given subtype.

Animals↗

Using physical-chemistry-based substitution models in phylogenetic analyses of HIV-1 subtypes.

HIV-1 subtype phylogeny is investigated using a previously developed computational model of natural amino acid site substitutions. This model, based on Boltzmann statistics and Metropolis kinetics, involves an order of magnitude fewer adjustable parameters than traditional substitution matrices and deals more effectively with the issue of protein site heterogeneity. When optimized for sequences of HIV-1 envelope (env) proteins from a few specific subtypes, our model is more likely to describe the evolutionary record for other subtypes than are methods using a single substitution matrix, even a matrix optimized over the same data. Pairwise distances are calculated between various probabilistic ancestral subtype sequences, and a distance matrix approach is used to find the optimal phylogenetic tree. Our results indicate that the relationships between subtypes B, C, and D and those between subtypes A and H may be closer than previously thought.

Gene Products, env↗

Peripheral nerve injury alters the alpha2 adrenoceptor subtype activated by clonidine for analgesia.

BACKGROUND: Previous studies suggest that the alpha adrenoceptor subtype is the target for spinally administered alpha -adrenergic agonists, clonidine, for pain relief. However, ST 91, a preferential alpha adrenoceptor subtype agonist, induces antinociception, and intrathecally administered alpha antisense oligodeoxynucleotide decreases antinociception induced by clonidine in the rat, suggesting non-A sites may be important as well. Therefore, the authors examined the subtype of alpha adrenoceptor activated by clonidine and ST 91 in normal rats and those with nerve injury-induced hypersensitivity. METHODS: The same mechanical stimulus was applied to normal rats and those following spinal nerve ligation, and the effect of intrathecal clonidine and ST 91 on withdrawal threshold to the stimulus was determined. To further examine subtypes, animals were spinally pretreated with vehicle, BRL 44408 (an alpha subtype-preferring antagonist), and ARC 239 (an alpha subtype-preferring antagonist). RESULTS: In normal animals, clonidine's effect was diminished by pretreatment with either antagonist, whereas ST 91's antinociceptive effect was solely blocked by pretreatment with ARC 239. In nerve-injured animals, the antihypersensitivity action of both clonidine and ST 91 was blocked by administration of ARC 239, whereas BRL 44408 was ineffective. CONCLUSIONS: These data agree with previous studies supporting that the alpha adrenoceptor is important to the antinociceptive effect of clonidine in normal animals. Nerve injury alters this and results in a total reliance on alpha adrenoceptors.

Adrenergic alpha-Agonists↗

Comparison of protein kinase C subtype expression between normal and aniridic human ocular surfaces: implications for limbal stem cell dysfunction in aniridia.

Frozen sections of corneoscleral buttons from normal and aniridic donors were stained with hematoxylin and periodic acid-Schiff, monoclonal antibodies AE-5 and AK-2 (to cornea-specific K3 and K12 keratins, respectively), and AM-3 (to conjunctival goblet cells) as well as with subtype-specific antibodies to seven different protein kinase C (PKC) subtypes, the signal transduction isoenzymes increasingly implicated in the regulation of cell growth and differentiation. Compared with the normal cornea, the aniridic cornea showed decreased AE-5 and AK-2 stainings, increased AM-3 staining, attenuated Bowman's membrane, invasion of new blood vessels, and limbal epithelial hyperplasia. In the normal tissue, the corneal epithelium expressed PKC alpha, lambda, and zeta; the limbal and conjunctival epithelia expressed additional PKC gamma. Conjunctival goblet cells expressed only PKC lambda. Within a given epithelium, different PKC subtypes had different cell-layer distributions. In the aniridic tissue, some of the four normally expressed subtypes were expressed in different cell layers, especially at the limbal region. PKC beta and PKC delta, which were normally weakly expressed, were markedly up-regulated. These results support the conclusion that the aniridic cornea does indeed manifest features of limbal stem cell deficiency with decreased corneal epithelial phenotype and increased conjunctival epithelial phenotype. Different capacities of proliferation and differentiation may be affected by the differential expression of PKC subtypes by different cell layers of normal ocular surface epithelia. The aberrant expression of PKC subtypes in aniridia may thus result in abnormal proliferation and differentiation noted in its ocular surface epithelia. Because limbal stem cells are the ultimate source of corneal proliferation and differentiation, we postulate that limbal deficiency in aniridia is a result of abnormal limbal stem cells.

Adult↗

Comparison of attention-deficit/hyperactivity disorder symptom subtypes in Ukrainian schoolchildren.

OBJECTIVE: This study used a parent-completed, DSM-IV-referenced rating scale to examine prevalence rates of attention-deficit/hyperactivity disorder (ADHD) behaviors and differences between subtypes in 10- to 12-year-old Ukrainian children. METHOD: During 1997, a total of 600 parents and children residing in Kyiv, Ukraine, and their teachers participated in extensive clinical assessments using standard Western measures. RESULTS: The screening prevalence rate of ADHD behaviors was 19.8%: 7.2% for inattentive (I), 8.5% for hyperactive-impulsive (HI), and 4.2% for combined (C). Post hoc comparisons indicated a number of significant (p < .05) group differences. Mothers of children with ADHD symptoms reported higher rates of disruptive behavior, negative mother-child interactions, and physical punishment than the non-ADHD group. Teachers rated children with ADHD as more hyperactive and inattentive, but only the HI subtype was rated more oppositional than non-ADHD students. The I subtype was less academically proficient and socially adept (but less likely to have behavior problems). The C subtype was the most behaviorally disruptive (mother ratings), and their fathers were more likely to be aggressive and abuse alcohol. The HI subtype also had problems with disruptive behavior but were less socially impaired. CONCLUSIONS: Although symptom prevalence rates are higher in Ukraine than the United States, this study provides additional evidence supporting DSM-IV ADHD subtypes as distinct clinical entities.

Analysis of Variance↗

Neuropsychological executive functions and DSM-IV ADHD subtypes.

OBJECTIVE: To evaluate and compare a focused set of component neuropsychological executive functions in the DSM-IV attention-deficit/hyperactivity disorder combined (ADHD-C) and inattentive (ADHD-I) subtypes. METHOD: The Stop task, Tower of London, Stroop task, Trailmaking Test, and output speed measures were completed by 105 boys and girls aged 7-12 classified as either DSM-IV ADHD-C (n = 46), ADHD-I (n = 18), or community control (n = 41). RESULTS: Both subtypes had deficits on output speed. A group x gender interaction was observed on the Stop task: boys with ADHD-C were impaired versus boys with ADHD-I, whereas girls in the two subtypes did not differ. The ADHD-C type had a deficit in planning. Neither ADHD group had a deficit in interference control per se, although they were slower than controls on the Stroop tasks. CONCLUSIONS: ADHD-I shares neuropsychological deficits with ADHD-C in the domain of output speed; on most domains the subtypes did not differ. Neuropsychological distinctions between these ADHD subtypes may be few, depending on which domain of executive functioning is assessed, and these distinctions differ by gender. In the case of boys, the two subtypes may be distinguished by the specificity of motor inhibition deficits to ADHD-C.

Attention Deficit Disorder with Hyperactivity↗

Characteristics and expression of transforming growth factor-beta receptor subtypes on vascular smooth muscle cells from spontaneously hypertensive rats.

OBJECTIVE: To investigate the characteristics and expression of transforming growth factor (TGF)-beta receptor subtypes on vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. METHODS: The effects of TGF-beta 1 on DNA synthesis were evaluated by [3H]-thymidine incorporation into quiescent VSMC plated at high (5 x 10(4) cells/cm2) or low (5 x 10(3) cells/cm2) cell density. Specific binding of TGF-beta to VSMC was assessed by incubation of the cells with [125I]-TGF-beta 1. Affinity labelling of receptor subtypes was achieved by exposure of the cells to [125I]-TGF-beta 1 and cross-linking with disuccimidyl suberate. RESULTS: VSMC from SHR displayed a biphasic DNA synthesis response to TGF-beta 1 at high cell density, with DNA synthesis stimulated by low concentrations of TGF-beta 1 but not by high concentrations, whereas at low cell density there was a small increase in DNA synthesis in response to TGF-beta 1. TGF-beta 1 inhibited DNA synthesis in VSMC from WKY rats at both high and low cell densities. Binding assays revealed that VSMC from SHR had a larger number of TGF-beta receptors and a higher affinity for TGF-beta at high and at low cell densities. The affinity labelling with [125I]-TGF-beta 1 revealed the presence of receptor subtypes with relative molecular masses of 280-300, 85, 70, 60 and 50 x 10(3) on vascular smooth muscle cells from both rat strains at high cell density. The abundance of the 85 x 10(3) molecular mass receptor subtype was greater in VSMC from SHR. The 85 x 10(3) molecular mass receptor subtype was not detected on VSMC from either strain at low cell density. CONCLUSION: The present results suggest a different expression of TGF-beta receptor subtypes on VSMC from SHR and WKY rats. These differences may account for the exaggerated proliferative response of VSMC from SHR to TGF-beta.

Animals↗

Angiotensin II AT2 receptor subtype: an uprising frontier in cardiovascular disease?

The renin-angiotensin system (RAS) plays a pivotal role in the regulation of fluid, electrolyte balance and blood pressure, and is a modulator of cellular growth and proliferation. Biological actions of RAS are linked to the binding of the effector molecule, angiotensin II (AngII), to specific membrane receptors, mostly the AT1 subtype and, to a lesser extent, other subtypes. Following the identification and characterization of the AT2 subtype receptor, it has been proposed that a complex interaction between AngII and its receptors may play an important role in the effects of RAS. In this paper current information on AngII subtype receptors--their structure, regulation and intracellular signalling--are reviewed, with a particular emphasis on the potential relevance for cardiovascular pathophysiology. In addition, we discuss modulation of expression of the AT2 receptor and its interaction with the AT1 receptor subtype, as well as the potential effects of this receptor on blood pressure regulation. A better understanding of the integrated effects of the AngII subtype receptors may help to elucidate the function of the RAS, as well as their participation in the mechanisms of cardiovascular disease and attendant therapeutic implications.

Animals↗

All developmental dyslexic subtypes display an elevated motion coherence threshold.

PURPOSE: Psychophysical studies indicate that many dyslexics have a motion-processing deficit. The purpose of this study was to determine whether elevated motion coherence thresholds correlate with the specific dyslexic subtypes as defined by the Boder classification scheme. METHODS: Twenty-one dyslexics (seven dyseidetics, six dysphonetics, and eight dysphoneidetics) and 19 age- and gender-matched controls participated in the study. The dyslexics were identified by an exclusionary approach and then subtyped with the Adult Dyslexia Test or the Dyslexia Determination Test. Motion coherence thresholds were determined with random dot kinematograms composed of signal dots and noise dots. Signal dots moved either left or right on each trial, whereas noise dots moved in random directions. The percentage of dots that comprised the signal was varied randomly on each trial (0 to 21% in 3% increments). Subjects guessed the direction of signal dot motion on each trial (two-alternative forced-choice task). A 75% correct threshold was determined with a Weibull equation fit to the psychometric function. RESULTS: All three dyslexic subtypes had elevated motion coherence thresholds (t-test; dyseidetics p = 0.01, dysphonetics p = 0.039, dysphoneidetics p = 0.048). CONCLUSION: Motion-coherence deficits are not correlated with a specific dyslexic subtype, but, rather, are common to all subtypes. However, some individuals in each of the dyslexic subtypes were found to have normal motion coherence thresholds, suggesting that other factors must be considered to predict the motion sensitivity deficits found in dyslexia.

Adolescent↗

What is the situation of human T cell lymphotropic virus type II (HTLV-II) in Africa? Origin and dissemination of genomic subtypes.

Human T cell lymphotropic virus type II (HTLV-II) and its two genomic subtypes, A and B, which differ by 3 to 6% at the nucleotide level (depending on the gene studied), were until recently considered to be endemic only in certain Indian tribes in the Americas and were therefore considered mainly as a "New World virus." First, the evidence of HTLV-II antibodies and later characterization of isolates from sex workers or individuals living in large West and Central African cities suggested that HTLV-II subtype A could have been imported recently in Africa. However, the findings of HTLV-II infection in two Pygmy populations living in remote areas of Zaire and Cameroon suggest that HTLV-II might have been in Africa for a very long time. Furthermore, the discovery of HTLV-II subtype B virus in some of these Pygmies, but also in other individuals from Zaire and within a family in Gabon for three generations, confirms the hypothesis of a very ancient presence of this HTLV-II subtype B on the African continent Recent data indicate also that there exist in Central Africa specific HTLV-II divergent strains including an HTLV-II B variant strain in Gabon. In the context of recent evidence for interspecies transmission in Central and West Africa of HTLV-I/simian T cell lymphotropic virus type I (STLV-I) strains, leading to the two major HTLV-I African subtypes, we would like to suggest that some STLV-II (closely related to HTLV-II subtype B) still exist or might have existed in Central/East Africa. The recent finding of quite divergent primate T cell lymphotropic viruses (PTLVs) in several Pygmy chimpanzees of Zairian origin (PTLV-PP1664 and STLV-PP) and in wild-caught baboons in Eritrea, Ethiopia (PTLV-L), also supports the complementary hypothesis of a yet to be discovered new HTLV-II-related virus in humans. Careful study of the indeterminate Western blot patterns present in some populations in Central Africa strongly suggests that such an exciting possibility exists, thus opening new avenues of research on both the history of primate retroviruses and that of early human groups.

Adolescent↗

Comparative analysis of HIV-1 viral load assays on subtype quantification: Bayer Versant HIV-1 RNA 3.0 versus Roche Amplicor HIV-1 Monitor version 1.5.

Quantification of HIV-1 subtypes is essential for appropriate clinical management. Whereas viral load assays were initially developed to accurately quantify subtype B, the recent worldwide spread of non-B subtypes and the introduction of treatment programs in regions with non-B subtypes have prompted adaptations of these assays. The Bayer Versant HIV-1 RNA 3.0 Assay (branched DNA [bDNA] 3.0) and the Roche Amplicor HIV-1 Monitor version 1.5 (Amplicor 1.5) assays are reported to quantify all subtypes in group M; however, evaluation of performance characteristics remains limited. In this study, we evaluated the accuracy and reliability of bDNA 3.0 and Amplicor 1.5 on multiple serially diluted viral isolates from HIV-1 group M, subtypes A through F. Testing was conducted on both assay systems in two independent laboratories. Comparative pansubtype quantification from regression analysis showed that quantification by bDNA 3.0 was approximately 0.3 log-fold lower than that by Amplicor 1.5. Comparative pansubtype accuracy analysis showed data points more closely distributed about their respective regression lines and thus showing greater reliability by bDNA 3.0 than by Amplicor 1.5.

Branched DNA Signal Amplification Assay↗

Uncommon mutations at residue positions critical for enfuvirtide (T-20) resistance in enfuvirtide-naive patients infected with subtype B and non-B HIV-1 strains.

Enfuvirtide (T-20) is the lead compound of the new class of antiretroviral drugs called fusion inhibitors. T-20 resistance-associated mutations located in the heptad repeat 1 (HR-1) domain of gp41 have been described in vitro and in clinical trials. In this study, the authors investigated the primary genotypic T-20 resistance in subtype B and non-B HIV-1 strains from patients at the beginning of their follow-up in the Luxembourg HIV Cohort as well as the emergence of primary resistance to T-20 in patients who had long-term infection with subtype B HIV-1 strains. HR-1 fragments including the gp41 amino acid 36-45, T-20-sensitive region were screened for amino acid variation. No classic T-20 resistance-associated mutations were identified in subtype B or non-B isolates. However, several uncommon mutations were found at residues 37, 39, and 42 for subtype B isolates and at residue 42 for a subtype non-B isolate. The results indicate that primary genotypic T-20 resistance seems to be rare in HIV-1, regardless of subtype or prior antiretroviral therapy (excluding fusion inhibitors). However, episodic variation within HR-1 can occur and needs further phenotypic evaluation in accurate fusion inhibitor resistance assays.

Anti-HIV Agents↗

Genetic contributions to the development of ADHD subtypes from childhood to adolescence.

OBJECTIVES: Little is known about how genes influence the development of symptoms included in the DSM-IV subtypes of attention-deficit/hyperactivity disorder (ADHD) from childhood to adolescence. The aim of this study was to examine genetic influences contributing to the development of hyperactive-impulsive symptoms and inattentive symptoms of ADHD from childhood to adolescence. METHOD: The sample included all 1,480 twin pairs born in Sweden between May 1985 and December 1986. Parents responded to mailed questionnaires on three occasions, when the twins were 8 to 9, 13 to 14, and 16 to 17 years old. The authors used dimensional scales of hyperactivity-impulsivity and inattention derived from a checklist of items based on the DSM symptoms of ADHD. RESULTS: Symptoms of hyperactivity-impulsivity declined with increasing age, whereas there was no decline in symptoms of inattention. Persistent genetic influences explain between 45% and 90% of the total genetic variance in hyperactivity-impulsivity and inattention across age. Persistent genetic variance was primarily operating across subtypes, even though persistent subtype-specific influences were also significant. CONCLUSIONS: The finding of persistent cross-subtype (i.e., combined) and persistent subtype-specific genetic influences (i.e., primarily hyperactive-impulsive and primarily inattentive) are in line with a genetic basis for the DSM-IV classification of ADHD subtypes.

Adolescent↗

The ectodomains but not the transmembrane domains of the fusion proteins of subtypes A and B avian pneumovirus are conserved to a similar extent as those of human respiratory syncytial virus.

The fusion glycoprotein (F(B)) gene of five strains of the B subtype of avian pneumovirus (APV; turkey rhinotracheitis virus) has been sequenced. The length of the F(B) protein was 538 amino acids, identical to that of the F protein of subtype A virus, with which it had 74% and 83% overall nucleotide and deduced amino acid identities, respectively. The F(B) and F(A) ectodomains had 90% amino acid identity, very similar to the 91% identity between the ectodomains of the F proteins of subtype A and B human respiratory syncytial virus (HRSV). As with HRSV, the F2 polypeptide was less conserved (83% identity) than F1 (94%). In contrast to the ectodomain, the transmembrane and cytoplasmic domains of the two APV subtypes were much less conserved (30% and 48% identity, respectively) than those of HRSV (92% and 87%, respectively). Comparisons within all the genera of the Paramyxoviridae (Pneumovirus, Morbillivirus, Paramyxovirus and Rubullavirus) show that low amino acid identity between F protein transmembrane domains is a feature of different species of virus rather than of strain differences. This may indicate that the two subtypes of APV have evolved in different geographical regions and/or different avian species. This is the first report of an F gene sequence from a subtype B APV.

Amino Acid Sequence↗

Molecular characterization of a complex, recombinant human immunodeficiency virus type 1 (HIV-1) isolate (A/G/J/K/?): evidence to support the existence of a novel HIV-1 subtype.

Recombination is one of several factors that contribute to the great genetic diversity of human immunodeficiency virus type 1 (HIV-1). In the current study, analysis of the full-length genome of a novel complex mosaic HIV-1 isolate (99GR303) from a Greek sailor who was possibly infected in Sierra Leone, Africa is presented. The 99GR303 isolate was found to comprise genomic regions belonging to subtypes A, G, J and K as well as of regions of a subtype that remains unclassified. For a partial region of env as well as vpr, no apparent similarity to the known HIV-1 subtypes or to any of the circulating recombinant forms was found. In fact, in the partial env gene, including the C2-V3 region, the 99GR303 isolate formed a new clade, suggesting the existence of an additional HIV-1 subtype. Thus, novel recombinants embody partial genomic regions which may have originated either from subtypes that existed in the past and became extinct or from contemporary subtypes that are extremely rare.

Acquired Immunodeficiency Syndrome↗