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PubMed1984

Homonyms, synonyms and mutations of the sequence/structure vocabulary.

Calladine (1982) proposed that steric repulsion between adjacent purines on opposite helix backbones accounts for the local variation seen in four helical parameters. By defining simple sum functions based on Calladine 's proposal, Dickerson (1983) has taken what he terms "the first step in establishing a sequence/structure vocabulary". In this letter we analyze the implications of the Calladine - Dickerson model with regard to " homonyms ", "synonyms" and mutations. Specifically, we (1) show that because of the number of adjacent helical positions affected by one transversion, two purine-pyrimidine sequences may be similar at the sequence level yet be very different structurally ( homonyms ); (2) list all sequences which, though different at the sequence level, share adjacent structural parameter values (synonyms); and (3) use two simple statistical measures to show that transversion mutations occurring between a purine and a pyrimidine (5'----3' on the same strand) are in general less disruptive of local helical structure than transversions occurring between a pyrimidine and purine. On the assumption that they are not inconsistent with experimental findings, we discuss the significance of these implications.

Base Sequence↗
PubMed1999

Examination of the selective pressures on a live PRRS vaccine virus.

We determined the ORF5 and 7 sequences of 20 pathogenic revertants of a live PRRSV vaccine. The sequence analysis confirmed all 20 isolates to be of vaccine origin. Having established that clonal introduction of American (vaccine) PRRS virus had occurred in Denmark, we could perform analysis of the selective pressure this attenuated virus had experienced during reversion. An analysis of nucleotide mutations showed a similar rate of mutations in the two genes (ORF5 and 7). However, non-synonymous mutations in ORF7 were eliminated by purifying selection. In contrast, non-synonymous mutations in ORF5 were tolerated or even selected for. The cDNA sequencing of the 20 vaccine virus revertants identified two single nucleotide mutations located in ORF5 and in ORF6 that we suggest are involved or at least linked to the attenuation of the vaccine virus and to the subsequent reversion to virulence.

Amino Acid Sequence↗
PubMed2002

Yersinia enterocolitica type III secretion: mutational analysis of the yopQ secretion signal.

Pathogenic Yersinia spp. secrete Yop proteins via the type III pathway. yopQ codons 1 to 15 were identified as a signal necessary and sufficient for the secretion of a fused reporter protein. Frameshift mutations that alter codons 2 to 15 with little alteration of yopQ mRNA sequence do not abolish type III transport, suggesting a model in which yopQ mRNA may provide a signal for secretion (D. M. Anderson and O. Schneewind, Mol. Microbiol. 31:1139-1148, 2001). In a recent study, the yopE signal was truncated to codons 1 to 12. All frameshift mutations introduced within the first 12 codons of yopE abolished secretion. Also, multiple synonymous mutations that changed the mRNA sequence of yopE codons 1 to 12 without altering the amino acid sequence did not affect secretion. These results favor a model whereby an N-terminal signal peptide initiates YopE into the type III pathway (S. A. Lloyd et al., Mol. Microbiol. 39:520-531, 2001). It is reported here that codons 1 to 10 of yopQ act as a minimal secretion signal. Further truncation of yopQ, either at codon 10 or at codon 2, abolished secretion. Replacement of yopQ AUG with either of two other start codons, UUG or GUG, did not affect secretion. However, replacement of AUG with CUG or AAA and initiating translation at the fusion site with npt did not permit Npt secretion, suggesting that the translation of yopQ codons 1 to 15 is a prerequisite for secretion. Frameshift mutations of yopQ codons 1 to 10, 1 to 11, and 1 to 12 abolished secretion signaling, whereas frameshift mutations of yopQ codons 1 to 13, 1 to 14, and 1 to 15 did not. Codon changes at yopQ positions 2 and 10 affected secretion signaling when placed within the first 10 codons but had no effect when positioned in the larger fusion of yopQ codons 1 to 15. An mRNA mutant of yopQ codons 1 to 10, generated by a combination of nine synonymous mutations, was defective in secretion signaling, suggesting that the YopQ secretion signal is not proteinaceous. A model is discussed whereby the initiation of YopQ polypeptide into the type III pathway is controlled by properties of yopQ mRNA.

3' Untranslated Regions↗
PubMed1999

Sequence evolution of the CCR5 chemokine receptor gene in primates.

The chemokine receptor CCR5 can serve as a coreceptor for M-tropic HIV-1 infection and both M-tropic and T-tropic SIV infection. We sequenced the entire CCR5 gene from 10 nonhuman primates: Pongo pygmaeus, Hylobates leucogenys, Trachypithecus francoisi, Trachypithecus phayrei, Pygathrix nemaeus, Rhinopithecus roxellanae, Rhinopithecus bieti, Rhinopithecus avunculus, Macaca assamensis, and Macaca arctoides. When compared with CCR5 sequences from humans and other primates, our results demonstrate that: (1) nucleotide and amino acid sequences of CCR5 among primates are highly homologous, with variations slightly concentrated on the amino and carboxyl termini; and (2) site Asp13, which is critical for CD4-independent binding of SIV gp120 to Macaca mulatta CCR5, was also present in all other nonhuman primates tested here, suggesting that those nonhuman primate CCR5s might also bind SIV gp120 without the presence of CD4. The topologies of CCR5 gene trees constructed here conflict with the putative opinion that the snub-nosed langurs compose a monophyletic group, suggesting that the CCR5 gene may not be a good genetic marker for low-level phylogenetic analysis. The evolutionary rate of CCR5 was calculated, and our results suggest a slowdown in primates after they diverged from rodents. The synonymous mutation rate of CCR5 in primates is constant, about 1.1 x 10(-9) synonymous mutations per site per year. Comparisons of Ka and Ks suggest that the CCR5 genes have undergone negative or purifying selection. Ka/Ks ratios from cercopithecines and colobines are significantly different, implying that selective pressures have played different roles in the two lineages.

Animals↗
PubMed1998

Evolution of hypervariable region 1 of hepatitis C virus in primary infection.

The hypervariable region 1 (HVR-1) of the putative envelope encoding E2 region of hepatitis C virus (HCV) RNA was analyzed in sequential samples from three patients with acute type C hepatitis infected from different sources to address (i) the dynamics of intrahost HCV variability during the primary infection and (ii) the role of host selective pressure in driving viral genetic evolution. HVR-1 sequences from 20 clones per each point in time were analyzed after amplification, cloning, and purification of plasmid DNA from single colonies of transformed cells. The intrasample evolutionary analysis (nonsynonymous mutations per nonsynonymous site [Ka], synonymous mutations per synonymous site [Ks], Ka/Ks ratio, and genetic distances [gd]) documented low gd in early samples (ranging from 2. 11 to 7.79%) and a further decrease after seroconversion (from 0 to 4.80%), suggesting that primary HCV infection is an oligoclonal event, and found different levels and dynamics of host pressure in the three cases. The intersample analysis (pairwise comparisons of intrapatient sequences; rKa, rKs, rKa/rKs ratio, and gd) confirmed the individual features of HCV genetic evolution in the three subjects and pointed to the relative contribution of either neutral evolution or selective forces in driving viral variability, documenting that adaptation of HCV for persistence in vivo follows different routes, probably representing the molecular counterpart of the viral fitness for individual environments.

Adolescent↗
PubMed2000

Viral genetic heterogeneity in HIV-1-infected individuals is associated with increasing use of HAART and higher viremia.

OBJECTIVE: To assess the correlation between the outgrowth of mutant viruses (viral genetic heterogeneity), highly active antiretroviral therapy (HAART), and plasma HIV-1 RNA in a population-based observational cohort study. DESIGN: The study population consisted of 42 HIV-1-infected individuals receiving at least two nucleotide reverse transcriptase (RT) inhibitors and one or more protease inhibitors at study entry. There were no restrictions on antiretroviral therapy after enrollment. METHODS: Plasma samples were obtained from subjects at baseline, at therapy changes, and at quarterly intervals for quantitation of HIV-1 RNA levels and for sequence determination of the entire protease coding region and the first 235 codons of the reverse transcriptase coding region. Data were analyzed using the generalized estimating equation method for longitudinal data and using linear regression analysis. RESULTS: With increased time on HAART there were significant increases in the number of total HIV-1 mutations in the regions sequenced (P = 0.010). There were significant correlations between the increases in the plasma HIV-1 RNA levels and the numbers of total mutations and reverse transcriptase mutations (P = 0.007 and 0.021, respectively). CONCLUSIONS: The number of HIV-1 mutations increased over time. Failure of HAART in this study population was correlated with outgrowth of virus with numerous mutations in the reverse transcriptase and protease coding regions. Phenotypic results correlated with genotypic results, showing decreased susceptibility to antiretrovirals over time in the majority of this population during HAART. Both synonymous and non-synonymous mutations were observed, with a higher incidence of non-synonymous mutations occurring at codons associated with drug resistance.

Adult↗
PubMed2024

A novel splice-altering TNC variant (c.5247A > T, p.Gly1749Gly) in an Chinese family with autosomal dominant non-syndromic hearing loss.

BACKGROUND: This study aims to analyze the pathogenic gene in a Chinese family with non-syndromic hearing loss and identify a novel mutation site in the TNC gene. METHODS: A five-generation Chinese family from Anhui Province, presenting with autosomal dominant non-syndromic hearing loss, was recruited for this study. By analyzing the family history, conducting clinical examinations, and performing genetic analysis, we have thoroughly investigated potential pathogenic factors in this family. The peripheral blood samples were obtained from 20 family members, and the pathogenic genes were identified through whole exome sequencing. Subsequently, the mutation of gene locus was confirmed using Sanger sequencing. The conservation of TNC mutation sites was assessed using Clustal Omega software. We utilized functional prediction software including dbscSNV_AdaBoost, dbscSNV_RandomForest, NNSplice, NetGene2, and Mutation Taster to accurately predict the pathogenicity of these mutations. Furthermore, exon deletions were validated through RT-PCR analysis. RESULTS: The family exhibited autosomal dominant, progressive, post-lingual, non-syndromic hearing loss. A novel synonymous variant (c.5247A > T, p.Gly1749Gly) in TNC was identified in affected members. This variant is situated at the exon-intron junction boundary towards the end of exon 18. Notably, glycine residue at position 1749 is highly conserved across various species. Bioinformatics analysis indicates that this synonymous mutation leads to the disruption of the 5' end donor splicing site in the 18th intron of the TNC gene. Meanwhile, verification experiments have demonstrated that this synonymous mutation disrupts the splicing process of exon 18, leading to complete exon 18 skipping and direct splicing between exons 17 and 19. CONCLUSION: This novel splice-altering variant (c.5247A > T, p.Gly1749Gly) in exon 18 of the TNC gene disrupts normal gene splicing and causes hearing loss among HBD families.

Adult↗
PubMed1998

Hypermutability and silent mutations in human carcinogenesis.

Silent or synonymous mutations are nucleotide changes which do not result in an amino acid change. Such alterations make up approximately 4% of the total TP53 mutations in a database of almost 10,000 mutations. Insofar as these changes do not confer a selective advantage, silent mutations make it possible to estimate an unbiased mutation frequency. Since this frequency is at least 100 times higher than would be expected for normal tissue, tumors must be hypermutable. In addition, a class of tumors may be supermutable with a mutation frequency comparable to that observed in the generation of immune diversity.

Chromosome Aberrations↗
PubMed2025

SARS-CoV-2 genomic diversity and within-host evolution in individuals with persistent infection in the UK: an observational, longitudinal, population-based surveillance study.

BACKGROUND: Persistent SARS-CoV-2 infections in hospitalised immunocompromised individuals are known to facilitate accelerated within-host viral evolution, potentially contributing to the emergence of highly divergent variants. However, little is known about the evolutionary dynamics and transmission risks of persistent infections in the general population. We aimed to characterise the within-host evolution of SARS-CoV-2 during persistent infections identified through a large community surveillance study. METHODS: We used data from the Office for National Statistics COVID-19 Infection Survey (ONS-CIS), a large-scale, longitudinal, population-based surveillance study conducted in the UK from April, 2020, to March, 2023. For this analysis, we focused on infections with high viral load (cycle threshold &#x2264;30) and available genome sequences, from seven major SARS-CoV-2 lineages (alpha, delta, BA.1, BA.2, BA.4, BA.5, and XBB). ONS-CIS participants were randomly selected from the general population and tested regularly by RT-PCR, regardless of symptoms. We defined persistent infections as those with sustained or rebounding high viral RNA titres for 26 days or longer. We examined associated host characteristics and used raw sequence data to identify de novo mutations and estimate within-host synonymous and non-synonymous evolutionary rates across the SARS-CoV-2 genome. FINDINGS: Between Nov 2, 2020, and March 21, 2023, we identified 576 persistent infections with at least two sequences, including 11 alpha, 106 delta, 102 BA.1, 204 BA.2, 16 BA.4, 133 BA.5, and 4 XBB. Persistent infections were more common in males than females (p<0&#xb7;0001) and individuals older than 60 years (p=0&#xb7;0027). The median within-host genome-wide evolutionary rate was 7&#xb7;9&#x2009;&#xd7;&#x2009;10-4 substitutions per site per year (IQR 7&#xb7;0-9&#xb7;0&#x2009;&#xd7;&#x2009;10-4), with high inter-individual variability driven largely by non-synonymous mutations, particularly in the N-terminal and receptor-binding domains of the spike protein. Longer infection duration was associated with higher evolutionary rates, while no associations were found with age, sex, vaccination status, previous infection, or virus lineage. We found no clear evidence of transmission beyond the first month of infection in any of the 84 persistent infections lasting 56 days or longer. In total, we identified 379 recurrent mutations, including many with known or predicted negative fitness effects and low prevalence at the population level, as well as de novo reversions to the Wuhan-Hu-1 reference sequence, which were likely under positive selection within those individuals. INTERPRETATION: This study highlights the heterogeneous nature of within-host SARS-CoV-2 evolution in individuals with persistent infection in the community. Notably, a small subset of persistent infections with high viral loads underwent accelerated viral evolution or recurrently acquired hallmark mutations found in novel variants. In addition, onward transmission from a persistent infection during the later stages of infection is likely to be rare. These insights have important implications for prioritising genomic surveillance and managing patients with persistent infections. FUNDING: Department of Health and Social Care.

Humans↗
PubMed2001

Screening breast cancer patients for ATM mutations and polymorphisms by using denaturing high-performance liquid chromatography.

All 62 coding exons of the ATM gene, along with 10-20 bases of the intronic region flanking each exon, were screened for DNA base sequence alterations by using denaturing high-performance liquid chromatography (DHPLC) in a series of 52 breast cancer patients. Six (12%) of these patients exhibited a total of eight different novel germ-line mutations that do not represent common polymorphisms. Of these, three patients possessed four nonconservative missense mutations while two conservative missense and two synonymous mutations were detected in the other three patients. In addition, 43 patients were found to have a total of 141 DNA sequence variations representing 21 different common polymorphisms and rare variants. An analysis of the relationship between the presence of a novel ATM mutation and either patient demographics or tumor properties demonstrated a significant difference between African Americans (3/7 = 43%) and other ethnic groups (3/45 = 7%, P = 0.026). None of the other characteristics examined was found to be related to mutation status.

Adult↗
PubMed2026

Wastewater-based sequencing of respiratory syncytial virus to investigate lineage dynamics and antigenic site mutations: a retrospective genomic epidemiology study.

BACKGROUND: Respiratory syncytial virus (RSV) infections pose a substantial health burden, particularly for clinically vulnerable populations such as infants and older adults. Although novel immunoprophylactic interventions show promise in providing protection, many countries may not have robust surveillance systems to monitor circulating RSV lineages and detect mutations that might reduce the effectiveness of these new interventions. We aimed to assess the diversity and temporal dynamics of circulating RSV lineages in urban populations through amplicon-based sequencing and analysis of wastewater extracts. METHODS: In this prospective observational wastewater-based genomic surveillance study, 32 raw influent 24-h composite samples were collected during the 2022-23 and 2023-24 RSV seasons from both Zurich and Geneva, Switzerland. We applied an RSV subtype-specific amplicon-based sequencing approach to obtain RSV-A and RSV-B sequences from all 64 samples. Mutations relative to reference genomes were identified at positions with read depth above 30. Relative abundances of RSV lineages were estimated from frequencies of lineage-signature mutations, present in greater than 90% of publicly available sequences of that lineage. FINDINGS: Relative abundances of RSV-B (2022-23) and RSV-A (2023-24) lineages were estimated over the two RSV seasons. During the 2022-23 season, the RSV-B B.D.E.1 lineage prevailed in both cities. In the 2023-24 season, multiple RSV-A lineages cocirculated, including A.D.1, A.D.3, A.D.5, and their sub-lineages. Identification and frequency estimation of mutations showed low-frequency, non-synonymous mutations in antigenic sites on the fusion gene of both RSV-A and RSV-B, some of which have not been reported in clinical sequences. The primary outcome was identification and relative abundance of RSV lineages in wastewater samples. INTERPRETATION: These findings show the potential of wastewater-based genomic surveillance to identify and track circulating RSV lineages and clinically relevant mutations. As novel RSV immunoprophylaxis measures are introduced in upcoming RSV seasons, wastewater-derived genomic RSV data provide a valuable baseline for understanding RSV diversity and future viral evolution under increased immunological pressure. FUNDING: This study was funded by the Swiss National Science Foundation and in part by the National Institute Of Allergy And Infectious Diseases of the National Institutes of Health. Funding for sample collection and processing was provided by the Swiss Federal Office of Public Health.

Humans↗
PubMed2000

Photoreactivation does not alter ras and p53 mutation spectra in ultraviolet radiation-induced corneal sarcomas of Monodelphis domestica.

When chronically exposed to ultraviolet radiation (UV), opossums of the species Monodelphis domestica develop corneal sarcomas at high frequency. Post-UV exposure to photoreactivating light enhances repair of UV-induced pyrimidine dimers and suppresses, but does not abrogate, corneal tumor development. We compared mutation spectra in ras and p53 genes in 32 eye tumors from Monodelphis exposed to UV alone and in 25 tumors from Monodelphis exposed to UV followed by photoreactivation in order to identify the particular types of mutation suppressed by enhanced repair of pyrimidine dimers. Mutations were detected by polymerase chain reaction amplification followed by direct sequencing or by "cold" single-strand conformational polymorphism analysis. The overall frequency of mutations was low, and there was no statistically significant difference between the two groups of tumors in the frequency or type of mutation. All mutations occurred at dipyrimidine sites, and most were C to T or CC to TT mutations, the hallmark UV-induced mutations. Hotspots of p53 mutation identified in a previous study of invasive tumors were absent, and mutations identified in the present study included synonymous mutations not previously detected. The difference in stage of the tumors examined is believed to account for these differences. The preponderance of signature UV mutations in p53 and ras genes confirm that UV is the proximate carcinogen for these tumors. The low incidence of mutations suggest that neither ras activation nor p53 inactivation is essential for tumor formation. Mutations attributable specifically to pyrimidine dimer formation could not be identified.

Animals↗
PubMed2001

[Characterization of rpoB mutation in rifampin - resistant clinical Mycobacterium tuberculosis isolates from China].

OBJECTIVE: To elucidate the characterization of rpoB mutation in rifampin - resistant clinical isolates of Mycobacterium tuberculosis isolates from China. METHODS: 588 bp DNA fragment of rpoB gene including 81 bp code region (rifampin resistance determination region, RRDR) was sequenced. 242 strains of Mycobacterium tuberculosis, including 193 rifampin - resistant strains and 46 rifampin - susceptible strains and 3 artificially induced rifampin - resistant strains were sequenced. RESULTS: 89.1% (172/193) rifampin - resistant strains had rpoB gene mutations in RRDR, no mutation was found in rifampin - susceptible strains. 46.1% rifampin - resistant strains had mutations located at 531-Ser; 17.1% strains had mutations located at 526-His; Combinative mutation rate was 12.4%; 4 strains had synonymous mutations; No deletion or insertion mutation was found among all strains. High level rifampin resistant strains (250 microgram/ml rifampin resistant) had higher mutation frequency at 531 - Ser than low level rifampin resistant strains (50 microgram/ml rifampin resistant) (P < 0.05). CONCLUSIONS: About 90% rifampin resistant clinical strains of Mycobacterium tuberculosis from China had rpoB mutations; 531-Ser and 526 - His were the most common positions to be substituted, the added mutation rate was about 46%; High level rifampin resistant strains had a higher frequency of 531-Ser mutation than low level rifampin resistant strains; No insertion or deletion mutation was found in these specimens; DNA sequencing is significant in drug choosing for tuberculosis treatment.

Antibiotics, Antitubercular↗
PubMed1997

Ancient mtDNA sequences in the human nuclear genome: a potential source of errors in identifying pathogenic mutations.

Nuclear-localized mtDNA pseudogenes might explain a recent report describing a heteroplasmic mtDNA molecule containing five linked missense mutations dispersed over the contiguous mtDNA CO1 and CO2 genes in Alzheimer's disease (AD) patients. To test this hypothesis, we have used the PCR primers utilized in the original report to amplify CO1 and CO2 sequences from two independent rho degrees (mtDNA-less) cell lines. CO1 and CO2 sequences amplified from both of the rho degrees cells, demonstrating that these sequences are also present in the human nuclear DNA. The nuclear pseudogene CO1 and CO2 sequences were then tested for each of the five "AD" missense mutations by restriction endonuclease site variant assays. All five mutations were found in the nuclear CO1 and CO2 PCR products from rho degrees cells, but none were found in the PCR products obtained from cells with normal mtDNA. Moreover, when the overlapping nuclear CO1 and CO2 PCR products were cloned and sequenced, all five missense mutations were found, as well as a linked synonymous mutation. Unlike the findings in the original report, an additional 32 base substitutions were found, including two in adjacent tRNAs and a two base pair deletion in the CO2 gene. Phylogenetic analysis of the nuclear CO1 and CO2 sequences revealed that they diverged from modern human mtDNAs early in hominid evolution about 770,000 years before present. These data would be consistent with the interpretation that the missense mutations proposed to cause AD may be the product of ancient mtDNA variants preserved as nuclear pseudogenes.

Alzheimer Disease↗
PubMed1994

An application of population genetic theory to synonymous gene sequence evolution in the human immunodeficiency virus (HIV).

A population genetic model is developed and then applied to the synonymous gene sequence variation observed in samples of the Human Immunodeficiency Virus Type 1 (HIV-1). The samples, which were taken from several previous studies, contain sequences of the envelope glycoprotein gene (gp 120) of HIV-1. This analysis suggests that the viral population within an infected patient at any specific time is likely to be composed of close relatives. The viruses in a sample are likely to share a recent common ancestor probably due to consistent positive selection for non-synonymous mutations coupled with low recombination in this region of the genome. There is no substantial difference in synonymous evolutionary rate between samples of sequences obtained from Peripheral Blood Mononucleate Cells (PBMCs) and samples taken from blood plasma. This is likely to be due to the high rate of migration between these 2 HIV subpopulations. The mutation rate for the genetic region examined is estimated at 9.20 x 10(-4) per site per month. Under the assumptions of the estimation procedure, this estimate can be bounded between 8.50 and 9.91 x 10(-4) with 95% confidence. When coupled with direct estimates of mutation rate, the rate of synonymous evolution suggests that the mean number of generations per month for HIV-1 in vivo is between 1 and 4.

Base Sequence↗
PubMed1981

Novel patterns of ultraviolet mutagenesis and Weigle reactivation in Staphylococcus aureus and phage phi 11.

The effects of u.v. irradiation on the survival of Staphylococcus aureus and its phage phi 11 were studied. The recA and uvr mutations affected their survival in a similar way to synonymous mutations in Escherichia coli. Weigle reactivation (W-reactivation) of phi 11 occurred in wild-type S. aureus and in a uvr mutant but to a lesser extent than has been found for phage lambda in E. coli. Reactivation was recA-dependent and was accompanied by u.v.-induced mutagenesis in a temperature-sensitive mutant of phi 11. Bacterial mutation to streptomycin resistance was induced by u.v. and was also recA-dependent. In S. aureus, as in E. coli, u.v. was a more effective mutagen in the uvr genetic background. However, a dose-squared response for u.v.-induced mutation of wild-type and uvr strains of S. aureus to streptomycin resistance, and of a trp auxotroph to tryptophan independence, was found only with u.v. doses below 1 J m-2. We suggest that, in relation to the Uvr mechanism of DNA repair, u.v. mutagenesis in S. aureus involves both repairable and non-repairable lesions. As in E. coli, the uvr genetic background reduced the u.v. dose required for maximal W-reactivation of u.v.-irradiated phage. However, there was no enhancement of W-reactivation by post-irradiation broth incubation of S. aureus. Our results are compatible with a non-inducible mechanism for this phenomenon.

DNA Repair↗
PubMed1998

Molecular variation in the nucleoprotein gene (ORF7) of the porcine reproductive and respiratory syndrome virus (PRRSV).

The nucleoprotein gene (ORF7) of 15 European isolates of porcine reproductive and respiratory syndrome virus (PRRSV) was sequenced and compared with corresponding sequences of other PRRSV isolates (2 European and 13 American) and one isolate each of other arteriviruses (the lactate dehydrogenase elevating virus (LDV), the simian haemorrhagic fever virus (SHFV) and the equine arteritis virus (EAV)). Their phylogenetic relationships were established using neighbour-joining and parsimony methods. Four lineages (PRRSV, LDV, SHFV and EAV) were discriminated. Two genotypes of PRRSV, European and American, could be further identified. The European genotype of PRRSV was highly conserved. Analysis of the nucleotide and amino acid substitutions in PRRSV ORF7 revealed four stable regions, probably conserved because of their requirement for nucleocapsid function and/or structure. No constant mutations accumulation in the ORF7 could be determined precisely when either synonymous or non-synonymous mutations were studied. Passage of the European PRRSV in vivo had little influence on the ORF7 sequence: only a small number of synonymous substitutions in ORF7 was detectable, confirming its low variability.

Amino Acid Sequence↗