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PubMed2006

Reassortment and concerted evolution in banana bunchy top virus genomes.

The nanovirus Banana bunchy top virus (BBTV) has six standard components in its genome and occasionally contains components encoding additional Rep (replication initiation protein) genes. Phylogenetic network analysis of coding sequences of DNA 1 and 3 confirmed the two major groups of BBTV, a Pacific and an Asian group, but show evidence of web-like phylogenies for some genes. Phylogenetic analysis of 102 major common regions (CR-Ms) from all six components showed a possible concerted evolution within the Pacific group, which is likely due to recombination in this region. The CR-M of additional Rep genes is close to that of DNA 1 and 2. Comparison of tree topologies constructed with DNA 1 and DNA 3 coding sequences of 14 BBTV isolates showed distinct phylogenetic histories based on Kishino-Hasegawa and Shimodaira-Hasegawa tests. The results of principal component analysis of amino acid and codon usages indicate that DNA 1 and 3 have a codon bias different from that of all other genes of nanoviruses, including all currently known additional Rep genes of BBTV, which suggests a possible ancient genome reassortment event between distinctive nanoviruses.

Asia↗

PubMed2006

Evolutionary history and global spread of the emerging g12 human rotaviruses.

G12 rotaviruses were first detected in diarrheic children in the Philippines in 1987, but no further cases were reported until 1998. However, G12 rotaviruses have been detected all over the world in recent years. Here, we report the worldwide variations of G12 rotaviruses to investigate the evolutionary mechanisms by which they managed to spread globally in a short period of time. We sequenced the complete genomes (11 segments) of nine G12 rotaviruses isolated in Bangladesh, Belgium, Thailand, and the Philippines and compared them with the genomes of other rotavirus strains. Our genetic analyses revealed that after introduction of the VP7 gene of the rare G12 genotype into more common local strains through reassortment, a vast genetic diversity was generated and several new variants with distinct gene constellations emerged. These reassortment events most likely took place in Southeast Asian countries and spread to other parts of the world. The acquirement of gene segments from human-adapted rotaviruses might allow G12 to better propagate in humans and hence to develop into an important emerging human pathogen.

Evolution, Molecular↗

PubMed1981

5'-terminal nucleotide noncoding sequences of retroviruses: relatedness of two old world primate type C viruses and avian spleen necrosis virus.

Computer-assisted comparison of the 5'-terminal regions of mammalian type C viruses serves as a useful model of evolutionary divergence of noncoding nucleic acid sequences. It has led to the concept that regions of conserved nucleic acid sequences, the slowly divergent sequences, contain signals of translational, transcriptional, or integrative significance. Interspersed among the conserved regions are rapidly divergent sequences in which base changes, insertions, and deletions are especially prevalent. In the present study, CPC-1, a type C virus isolated from Colobus polykomos, was shown to be related to another Old World type C monkey virus, endogenous stump-tailed monkey virus, MAC-1, by analysis of their 5'-terminal nucleotide sequences. The 5'-terminal regions of CPC-1 and MAC-1 showed a 76% nucleotide correspondence and were of similar lengths, 132 and 127 nucleotides, respectively. Previous strong-stop analyses of other type C viruses have defined two subgroups: (i) Rauscher murine leukemia virus and gibbon ape leukemia virus and (ii) baboon endogenous virus and endogenous cat virus RD114. Based on the present sequence analysis of their 5'-terminal sequences, CPC-1 and MAC-1 formed a third subgroup. Computer-assisted comparison of the 5'-terminal sequences of CPC-1 and MAC-1 to the previously reported sequence of avian spleen necrosis virus (SNV) (Shimotohno et al., Nature [London] 285:550-554, 1980) showed SNV to be a member of that subgroup of mammalian type C viruses. Consistent with the inclusion of SNV in this subgroup of mammalian type C viruses, SNV was distantly related to other mammalian type C viruses. Interestingly, the SNV 5'-terminal sequences showed no significant evolutionary relationship by these criteria to the avian leukemia and sarcoma viruses. CPC-1, MAC-1, and SNV contained conserved regulatory signals in similar positions in their 5'-terminal RNA sequences analogous to those observed in other mammalian type C retroviruses. These sequences included the canonical AAUAAA sequence, a palindrome, a putative ribosome binding site, and an integration site. Some of these highly conserved subsequences were common to 3'- and 5'-terminal noncoding sequences of nonviral eucaryotic mRNA's (Efstratiadis et al., Cell 21:653-668, 1980). Thus, analysis and comparison of 5'-terminal nucleotide sequences have been useful in defining common functional signals and in extending the matrix of relationships among retroviruses.

Base Sequence↗

PubMed1983

Antigenic drift in influenza virus H3 hemagglutinin from 1968 to 1980: multiple evolutionary pathways and sequential amino acid changes at key antigenic sites.

Surveys of the antigenic properties of a wide range of variants of the H3N2 (Hong Kong) influenza virus subtype have revealed complex patterns of variants cocirculating during each of the main epidemic eras of the subtype. We determined hemagglutinin (HA) gene sequences for 14 isolates chosen to give the wildest possible spread of variant types. The addition of these data to existing HA gene sequence information for other variants provides a comprehensive picture of HA gene evolution during antigenic drift among H3N2 subtype viruses. The data reveal the existence of multiple evolutionary pathways during at least one period of development of the subtype and strikingly demonstrate that amino acid changes are limited to a small number of locations on the HA molecule during antigenic drift. The occurrence of sequential amino acid changes at key positions within these variable regions suggests that the HA structure has remained constant during subtype evolution so that only limited possibilities remain for further antigenic drift among H3N2 viruses.

Amino Acid Sequence↗

PubMed1984

Influenza C virus hemagglutinin: comparison with influenza A and B virus hemagglutinins.

The complete nucleotide sequence of the influenza C/California/78 virus RNA 4 was obtained by using cloned cDNA derived from the RNA segment. This gene is 2,071 nucleotides long and can code for a polypeptide of 654 amino acids. Although there are no convincing sequence homologies between RNA 4 and the hemagglutinin genes of influenza A and B viruses, we suggest, on the basis of structural features, that RNA 4 of the influenza C virus codes for the hemagglutinin. The structural features which are common to the hemagglutinins of influenza A, B, and C viruses include (i) a hydrophobic signal peptide, (ii) an arginine cleavage site between the hemagglutinin 1 and 2 subunits, (iii) hydrophobic regions at the amino and carboxyl termini of the hemagglutinin 2 subunit, and (iv) several conserved cysteine residues. Additional evidence that RNA 4 of influenza C virus codes for the hemagglutinin is that the tripeptide Ile-Phe-Gly, known to be present at the amino terminus of the hemagglutinin 2 subunit of influenza C virus, is encoded by RNA 4 at a point immediately adjacent to the presumptive arginine cleavage site. The lack of primary sequence homology between the influenza C virus hemagglutinin and the influenza A or B virus hemagglutinins, which all have similar functions, might be attributed to convergent rather than divergent evolution. However, the structural similarities among the influenza A, B, and C virus hemagglutinins strongly suggest that the three hemagglutinin genes have diverged from a common precursor.

Amino Acid Sequence↗

PubMed1985

Epstein-Barr virus genome may encode a protein showing significant amino acid and predicted secondary structure homology with glycoprotein B of herpes simplex virus 1.

We report significant sequence and predicted secondary structure homology between the herpes simplex virus 1 glycoprotein B (gB) and a protein predicted to be encoded by the BALF4 reading frame of Epstein-Barr virus (EBV). Homology was detectable at the DNA level and was highly significant at the protein level and when evolutionary substitution frequencies of amino acids in related proteins were taken into account. Hydropathic analyses predicted that the two proteins possess conserved N-terminal and C-terminal hydrophobic domains. The N-terminal hydrophobic domains share features in common with known cleavable membrane insertion signal sequences. The amino acid sequences of the C-terminal hydrophobic domains predict three adjacent membrane-spanning segments as had been previously predicted for gB. In an alignment of the two amino acid sequences, 247 of 903 gB residues had a matched pair in the BALF4 sequence, and 247 of 854 BALF4 residues were found to have a matched pair in the gB sequence. In addition, all 10 cysteine residues located outside the predicted signal sequence of both proteins were conserved, as were four predicted N-linked glycosylation sites. In all, 43% of the residues in the aligned sequences are predicted to possess equivalent secondary structures. gB is a virion envelope glycoprotein required for virus entry into cells. The domain of gB determining the rate of entry into cells has been mapped; the predicted structure of this domain in gB and the predicted EBV protein are almost identical. Similarly, the cytoplasmic domain of gB postulated to interact with submembrane proteins was also nearly identical in predicted structure to that of the EBV protein. These results suggest that EBV encodes a protein similar in structure and function to the herpes simplex virus 1 gB.

Amino Acid Sequence↗

PubMed1990

Polymerase errors accumulating during natural evolution of the glycoprotein gene of vesicular stomatitis virus Indiana serotype isolates.

We report the entire glycoprotein (G) gene nucleotide sequences of 26 vesicular stomatitis virus Indiana serotype (VSV IND) type 1 isolates from North and Central America. These sequences are also compared with partial G gene sequences of VSV IND type 2 (Cocal) and type 3 (Alagoas) viruses and the complete G gene sequences of the more distantly related VSV New Jersey (NJ) and Chandipura viruses. Phylogenetic analysis of the G gene sequences by maximum parsimony revealed four major lineages or subtypes within the classical VSV IND (type 1) viruses, each with a distinct geographic distribution. A high degree of VSV genetic diversity was found in Central America, with several virus subtypes of both VSV IND and NJ serotypes existing in this mainly enzootic disease region. Nineteen percent sequence variation but no deletions or insertions were evident within the 5' noncoding and the coding regions of the VSV IND type 1 G genes. In addition to numerous base substitutions, the 3' noncoding regions of these viruses also contained numerous base insertions and deletions. This resulted in striking variation in G gene sizes, with gene lengths ranging from 1,652 to 1,868 nucleotides. As the VSV IND type 1 subtypes have diverged from the common ancestor with the NJ subtypes, their G mRNAs have accumulated more 3' noncoding sequence inserts, ranging up to 303 nucleotides in length. These primarily consist of an imprecise reiteration of the sequence UUUUUAA, apparently generated by a unique polymerase stuttering error. Analysis of the deduced amino acid sequence differences among VSV IND type 1 viruses revealed numerous substitutions within defined antigenic epitopes, suggesting that immune selection may play a role in the evolution of these viruses.

Amino Acid Sequence↗

PubMed1990

Phosphoprotein and nucleocapsid protein evolution of vesicular stomatitis virus New Jersey.

The entire phosphoprotein (P) and nucleocapsid (N) protein gene sequences and deduced amino acid sequences for 18 selected vesicular stomatitis virus isolates representative of the natural genetic diversity within the New Jersey serotype are reported. Phylogenetic analysis of the data using maximum parsimony allowed construction of evolutionary trees for the individual genes and the combined N, P, and glycoprotein (G) genes of these viruses. Virtually identical rates of nucleotide substitutions were found for each gene, indicating that evolution of these genes occurs at essentially the same rate. Although up to 19 and 17% sequence differences were evident in the P and N genes, respectively, no variation in gene length or evidence of recombinational rearrangements was found. However, striking evolutionary differences were observed among the amino acid sequences of vesicular stomatitis virus New Jersey N, P, and G proteins. The N protein amino acid sequence was the most highly conserved among the different isolates, indicating strong functional and structural constraints. Conversely, the P protein amino acid sequences were highly variable, indicating considerably fewer constraints or greater evolutionary pressure on the P protein. Much of the remarkable amino acid variability of the P protein resided in a hypervariable domain located between amino acids 153 and 205. The variability within this region would be consistent with it playing a structural role as a spacer to maintain correct conformational presentation of the separate active domains of this multifunctional protein. In marked contrast, the adjacent domain I of the P protein (previously thought to be under little evolutionary constraint) contained a highly conserved region. The colocalization of a short, potentially functional overlapping open reading frame to this region may explain this apparent anomaly.

Amino Acid Sequence↗

PubMed1992

Evolution of the capsid protein genes of foot-and-mouth disease virus: antigenic variation without accumulation of amino acid substitutions over six decades.

The genetic diversification of foot-and-mouth disease virus (FMDV) of serotype C over a 6-decade period was studied by comparing nucleotide sequences of the capsid protein-coding regions of viruses isolated in Europe, South America, and The Philippines. Phylogenetic trees were derived for VP1 and P1 (VP1, VP2, VP3, and VP4) RNAs by using the least-squares method. Confidence intervals of the derived phylogeny (significance levels of nodes and standard deviations of branch lengths) were placed by application of the bootstrap resampling method. These procedures defined six highly significant major evolutionary lineages and a complex network of sublines for the isolates from South America. In contrast, European isolates are considerably more homogeneous, probably because of the vaccine origin of several of them. The phylogenetic analysis suggests that FMDV CGC Ger/26 (one of the earliest FMDV isolates available) belonged to an evolutionary line which is now apparently extinct. Attempts to date the origin (ancestor) of the FMDVs analyzed met with considerable uncertainty, mainly owing to the stasis noted in European viruses. Remarkably, the evolution of the capsid genes of FMDV was essentially associated with linear accumulation of silent mutations but continuous accumulation of amino acid substitutions was not observed. Thus, the antigenic variation attained by FMDV type C over 6 decades was due to fluctuations among limited combinations of amino acid residues without net accumulation of amino acid replacements over time.

Amino Acid Sequence↗

PubMed1994

Epstein-Barr virus infection induces expression in B lymphocytes of a novel gene encoding an evolutionarily conserved 55-kilodalton actin-bundling protein.

A novel human mRNA whose expression is induced over 200-fold in B lymphocytes by latent Epstein-Barr virus (EBV) infection was reverse transcribed, cloned, and sequenced. The mRNA is predicted to encode a protein containing four peptides which precisely match amino acid sequences from a previously identified 55-kDa actin-bundling protein, p55. In vitro translation of the cDNA results in a 55-kDa protein which binds to actin filaments in the presence of purified p55 from HeLa cells. The p55 mRNA is undetectable in non-EBV-infected B- and T-cell lines or in a myelomonocytic cell line (U937). Newly infected primary human B lymphocytes, EBV-transformed B-cell lines, latently infected Burkitt tumor cells expressing EBNA2 and LMP1, a chronic myelogenous leukemia cell line (K562), and an osteosarcoma cell line (TK143) contain high levels of p55 mRNA or protein. In EBV-transformed B cells, p55 localizes to perinuclear cytoplasm and to cell surface processes that resemble filopodia. The p55 mRNA is detected at high levels in spleen and brain tissues, at moderate levels in lung and placenta tissues, and at low levels in skeletal muscle, liver, and tonsil tissues and is undetectable in heart, kidney, pancreas, and bone marrow tissues. Immunohistochemical staining of human brain tissue demonstrates p55 localization to the perinuclear cytoplasm and dendritic processes of many, but not all, types of cortical or cerebellar neurons, to glial cells, and to capillary endothelial cells. In cultured primary rat neurons, p55 is distributed throughout the perinuclear cytoplasm and in subcortical filamentous structures of dendrites and growth cones. p55 is highly evolutionarily conserved since it shows 40% amino acid sequence identity to the Drosophila singed gene product and 37% identity to fascin, an echinoderm actin-bundling protein. The evolutionary conservation of p55 and its lack of extensive homology to other actin-binding proteins suggest that p55 has specific microfilament-associated functions in cells in which it is differentially expressed, including neural cells and EBV-transformed B lymphocytes.

Amino Acid Sequence↗

PubMed1995

Evolution of the feline-subgroup parvoviruses and the control of canine host range in vivo.

A related group of parvoviruses infects members of many different carnivore families. Some of those viruses differ in host range or antigenic properties, but the true relationships are poorly understood. We examined 24 VP1/VP2 and 8 NS1 gene sequences from various parvovirus isolates to determine the phylogenetic relationships between viruses isolated from cats, dogs, Asiatic raccoon dogs, mink, raccoons, and foxes. There were about 1.3% pairwise sequence differences between the VP1/VP2 genes of viruses collected up to four decades apart. Viruses from cats, mink, foxes, and raccoons were not distinguished from each other phylogenetically, but the canine or Asiatic raccoon dog isolates formed a distinct clade. Characteristic antigenic, tissue culture host range, and other properties of the canine isolates have previously been shown to be determined by differences in the VP1/VP2 gene, and we show here that there are at least 10 nucleotide sequence differences which distinguish all canine isolates from any other virus. The VP1/VP2 gene sequences grouped roughly according to the time of virus isolation, and there were similar rates of sequence divergence among the canine isolates and those from the other species. A smaller number of differences were present in the NS1 gene sequences, but a similar phylogeny was revealed. Inoculation of mutants of a feline virus isolate into dogs showed that three or four CPV-specific differences in the VP1/VP2 gene controlled the in vivo canine host range.

Amino Acid Sequence↗

PubMed1996

Molecular anatomy of mouse hepatitis virus persistence: coevolution of increased host cell resistance and virus virulence.

Persistent infection of murine astrocytoma (DBT) cells with mouse hepatitis virus (MHV) has been established. From this in vitro virus-host system, persistence is mediated at the level of cellular MHV receptor (MHVR) expression and increased virus virulence. MHV persistence selects for resistant host cell populations which abate virus replication. Reductions in MHVR expression were significantly associated with increased host resistance, and transfection of MHVR into resistant host cells completely restored the capacity of cells to support efficient replication of MHV strain A59. The emergence of resistant host cells coselected for variant viruses that had increased avidity for MHVR and also recognized different receptors for entry into resistant cells. These data illustrate that MHV persistence in vitro provides a model to identify critical sites of virus-host interaction at the cellular level which are altered during the evolution of host cell resistance to viral infection and the coevolution of virus virulence.

Animals↗

PubMed1997

Investigation of the dynamics of the spread of human immunodeficiency virus to brain and other tissues by evolutionary analysis of sequences from the p17gag and env genes.

The time of spread of human immunodeficiency virus type 1 (HIV-1) from lymphoid to nonlymphoid tissues in the course of infection was investigated by sequence comparisons of variants infecting a range of lymphoid and nonlymphoid tissues from three individuals with AIDS in the pl7gag gene and regions flanking the V1/V2 hypervariable regions. Phylogenetic analysis in both regions revealed several lineages in each individual that contained sequences from both lymphoid and nonlymphoid tissues such as the brain. This observation contrasts strongly with the previously described organ-specific sequences in the V3 region in this study population and other investigations. Although individual pairwise comparisons of relatively short sequences such as p17gag are subject to considerable stochastic error, we found that the diversity of gag sequences in variants from lymphoid tissue was consistently lower than that found among variants amplified from the brain. By estimating mean synonymous pairwise distances in the p17gag region, we were able to make an approximate calculation of the ages of populations in different tissues. Those from lymphoid tissue ranged from 2.65 to 5.6 years in the three study subjects, compared with 4.1 to 6.2 years for variants in the brain. Indeed, variants infecting the brain were no more closely related to each other than they were to variants infecting other tissues in the body. In two of the three individuals, these times of divergence indicate that infection of the brain may have occurred as an early event in the progression to disease, preceding the onset of AIDS by several years. This study is the first in which it was possible to estimate times of diversification in different tissues in vivo and is of importance in understanding the dynamics of the spread of HIV-1 into nonlymphoid tissues and its possible adaptation for replication in different cell types.

Acquired Immunodeficiency Syndrome↗

PubMed1997

In vivo sequence variability of human immunodeficiency virus type 1 envelope gp120: association of V2 extension with slow disease progression.

According to the rate of depletion of CD4 cell counts, we grouped 12 cases of human immunodeficiency virus type 1 (HIV-1) infection as 6 rapid (21.0 to 33.8 cells per microl per month) and 6 slow (0.9 to 7.9 cells per microl per month) progressors and determined the individual viral quasispecies patterns by sequencing the genome region encoding the V1, V2, and V3 loops of envelope protein. Although the quasispecies structures varied widely from one individual to another, a strong correlation was observed between a low rate of disease progression and a high degree of genetic diversity of HIV-1. Furthermore, the V2 loop extension was observed specifically in individuals with slow or no disease progression, whereas basic amino acid substitutions in V3 characteristic of a viral phenotype shift from non-syncytium inducing to syncytium inducing were observed in patients with advanced stages of disease regardless of their rate of disease progression. Studies with recombinant viruses suggested that elongation of V2 potentially restricts the capacity of HIV-1 to replicate in macrophages. Thus, our results suggest the association of distinct sequence features of both V3 and V2 with particular patterns of disease progression. Elongation of the V2 loop may be a good predictor of slow disease progression, while basic substitutions of V3 without elongation of V2 are characteristic of rapid progression.

Amino Acid Sequence↗

PubMed1998

Phylogenetic analysis of the entire genome of influenza A (H3N2) viruses from Japan: evidence for genetic reassortment of the six internal genes.

Nucleotide sequences of all eight RNA segments of 10 human H3N2 influenza viruses isolated during a 5-year period from 1993 to 1997 were determined and analyzed phylogenetically in order to define the evolutionary pathways of all genes in a parallel fashion. It was evident that the hemagglutinin and neuraminidase genes of these viruses evolved essentially in a single lineage and that amino acid changes accumulated sequentially with respect to time. In contrast, amino acid differences in the internal proteins were erratic and did not accumulate over time. Parallel analysis of the phylogenetic patterns of all genes revealed that the evolutionary pathways of the six internal genes were not linked to the surface glycoproteins. Genes coding for the basic polymerase-1, nucleoprotein, and matrix proteins of 1997 isolates were closest phylogenetically to those of earlier isolates of 1993 and 1994. Furthermore, all six internal genes of four viruses isolated in the 1995 epidemic season consistently divided into two distinct branch clusters, and two 1995 isolates contained PB2 genes apparently originating from those of viruses before 1993. It was apparent that the lack of correlation between the topologies of the phylogenetic trees of the genes coding for the surface glycoproteins and internal proteins was a reflection of genetic reassortment among human H3N2 viruses. This is the first evidence demonstrating the occurrence of genetic reassortment involving the internal genes of human H3N2 viruses. Furthermore, internal protein variability coincided with marked increases in the activity of H3N2 viruses in 1995 and 1997.

Amino Acid Sequence↗

PubMed1999

Search for the mechanism of genetic variation in the pro gene of human immunodeficiency virus.

To study the mechanism of evolution of the human immunodeficiency virus (HIV) protease gene (pro), we analyzed a database of 213 pro sequences isolated from 11 HIV type 1-infected patients who had not been treated with protease inhibitors. Variation in pro is restricted to rare variable bases which are highly diverse and differ in location among individuals; an average variable base appears in about 16% of individuals. The average intrapatient distance per individual variable site, 27%, is similar for synonymous and nonsynonymous sites, although synonymous sites are twice as abundant. The latter observation excludes selection for diversity as an important, permanently acting factor in the evolution of pro and leaves purifying selection as the only kind of selection. Based on this, we developed a model of evolution, both within individuals and along the transmission chain, which explains variable sites as slightly deleterious mutants slowly reverting to the better-fit variant during individual infection. In the case of a single-source transmission, genetic bottlenecks at the moment of transmission effectively suppress selection, allowing mutants to accumulate along the transmission chain to high levels. However, even very rare coinfections from independent sources are, as we show, able to counteract the bottleneck effect. Therefore, there are two possible explanations for the high mutant frequency. First, the frequency of coinfection in the natural host population may be quite low. Alternatively, a strong variation of the best-adapted sequence between individuals could be caused by a combination of an immune response present in early infection and coselection.

Base Sequence↗

PubMed1999

Evidence of recombination among enteroviruses.

Human enteroviruses consist of more than 60 serotypes, reflecting a wide range of evolutionary divergence. They have been genetically classified into four clusters on the basis of sequence homology in the coding region of the single-stranded RNA genome. To explore further the genetic relationships between human enteroviruses and to characterize the evolutionary mechanisms responsible for variation, previously sequenced genomes were subjected to detailed comparison. Bootstrap and genetic similarity analyses were used to systematically scan the alignments of complete genomic sequences. Bootstrap analysis provided evidence from an early recombination event at the junction of the 5' noncoding and coding regions of the progenitors of the current clusters. Analysis within the genetic clusters indicated that enterovirus prototype strains include intraspecies recombinants. Recombination breakpoints were detected in all genomic regions except the capsid protein coding region. Our results suggest that recombination is a significant and relatively frequent mechanism in the evolution of enterovirus genomes.

Enterovirus↗

PubMed1999

Strong selective pressure for evolution of an Epstein-Barr virus LMP2B homologue in the rhesus lymphocryptovirus.

Latent membrane protein 2B (LMP2B) is expressed during latent Epstein-Barr virus (EBV) infection, but little is known about its role. The goal of this study was to determine whether an LMP2B homologue is conserved in the rhesus monkey lymphocryptovirus (LCV). Both rhesus LCV LMP2A and LMP2B genes were cloned and sequenced. The rhesus LCV LMP2B gene is positionally conserved, and the EBNA-2 responsiveness and the bidirectional nature of the LMP1-LMP2B promoter have also been functionally conserved. However, this region of the genome encoding the LMP1, LMP1-LMP2B promoter, and LMP2B first exon demonstrates the most dramatic nucleotide sequence divergence between human and nonhuman LCV observed to date. Evolution of the rhesus LCV LMP2B promoter and transcript despite the dynamic nature of this genomic region reflects strong selective pressure for a yet-to-be-identified LMP2B function.

Amino Acid Sequence↗