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PubMed2003

Evolution of primate theta-defensins: a serpentine path to a sweet tooth.

Retrocyclins (ancestral human theta-defensins) are cyclic antimicrobial octadecapeptides that interfere with viral uptake and protect human cells from infection by T- and M-tropic strains of HIV-1 in vitro. As are other theta-defensins, retrocyclins are lectins that bind gp120, CD4, and galactosylceramide-all of which are implicated in HIV-1 uptake. Although theta-defensin mRNA transcripts are present in human bone marrow, spleen, thymus, testis, and skeletal muscle, a premature stop codon aborts their translation. We found six theta-defensin (DEFT) genes in the human genome; five on chromosome 8p23 and one on chromosome 1. All six of these pseudogenes, as well as their homologues in chimpanzees and gorillas, contained the same premature stop codon mutation. Whereas we found intact DEFT genes in DNA from several Old World Monkeys, Hylobates syndactylus (a lesser ape) and orangutans, no homologues were present in DNA from six New World Monkeys and five prosimians. We conclude that DEFT genes and theta-defensins arose in Old World Monkeys by mutation of a pre-existing alpha-defensin gene. Although intact DEFT genes survive in some nonhuman primates, our hominid ancestors lost their ability to produce theta-defensins after the orangutan and hominid lineages diverged. It is possible (but may be difficult to prove) that this mutation rendered our species more susceptible to infection by HIV-1.

Amino Acid Sequence↗

PubMed2003

Expression of estrogen receptor beta exon-deleted variant mRNAs in ovary and uterine endometrium.

Various estrogen receptor beta exon-deleted variant (ER-beta EDV) mRNAs were expressed in human ovary and uterine endometrium. Estrogen receptor beta (ER-beta) completely or partially deleted exon n is expressed as ER-beta EnDV or En'DV, respectively. The mRNAs for ER-beta single exon-deleted variant (EDV), ER-beta E2DV, E4DV, E5DV and E6DV; for ER-beta double exon-deleted variants, ER-beta E1'+2DV, E4+5DV and E5+6DV; and for ER-beta triple exon-deleted variants, ER-beta E2'+3+4DV and E4+5+6DV were detected. In ER-beta E2DV, E4+5DV, E5DV and E6DV mRNAs, the new stop codon is made in the exon following the deleted exon(s), and the new proteins may lack the corresponding domains. In ER-beta E1'+2DV, E2'+3+4DV, E4DV, E4+5+6DV and E5+6DV mRNAs, the original stop codon is still present, and the new proteins may conserve the new short amino acid sequences surrounding the deleted exons. ER-beta E1'+2DV, E2DV, E2'+3+4DV, E4DV, E4+5DV and E4+5+6 are unlikely to work as a transcription factors. On the other hand, ER-beta E5DV, E6DV and E5+6DV lack only the ligand-binding domain, and might work as dominant positive or negative factors. Therefore, ER-beta E5DV, E6DV and E5+6DV, constitutively expressed in human ovary and uterine endometrium might, in part regulate estrogen responsiveness.

Adult↗

PubMed2002

IntI2 integron integrase in Tn7.

Integrons can insert and excise antibiotic resistance genes on plasmids in bacteria by site-specific recombination. Class 1 integrons code for an integrase, IntI1 (337 amino acids in length), and are generally borne on elements derived from Tn5090, such as that found in the central part of Tn21. A second class of integron is found on transposon Tn7 and its relatives. We have completed the sequence of the Tn7 integrase gene, intI2, which contains an internal stop codon. This codon was found to be conserved among intI2 genes on three other Tn7-like transposons harboring different cassettes. The predicted peptide sequence (IntI2*) is 325 amino acids long and is 46% identical to IntI1. In order to detect recombination activity, the internal stop codon at position 179 in the parental allele was changed to a triplet coding for glutamic acid. The sequences flanking the cassette arrays in the class 1 and 2 integrons are not closely related, but a common pool of mobile cassettes is used by the different integron classes; two of the three antibiotic resistance cassettes on Tn7 and its close relatives are also found in various class 1 integrons. We also observed a fourth excisable cassette downstream of those described previously in Tn7. The fourth cassette encodes a 165-amino-acid protein of unknown function with 6.5 contiguous repeats of a sequence coding for 7 amino acids. IntI2*179E promoted site-specific excision of each of the cassettes in Tn7 at different frequencies. The integrases from Tn21 and Tn7 showed limited cross-specificity in that IntI1 could excise all cassettes from both Tn21 and Tn7. However, we did not observe a corresponding excision of the aadA1 cassette from Tn21 by IntI2*179E.

3' Untranslated Regions↗

PubMed1991

Emergence of and takeover by hepatitis B virus (HBV) with rearrangements in the pre-S/S and pre-C/C genes during chronic HBV infection.

We have shown, by analyzing serial serum samples from a chronic hepatitis B virus (HBV) carrier, the emergence of HBV DNA molecules with nucleotide rearrangements in the pre-S/S and pre-C/C genes. Serum samples were obtained at four different times (1983, 1985, 1988, and 1989) from an HBsAg- and HBeAg-positive carrier with chronic hepatitis. The polymerase chain reaction was used to amplify the pre-S/S and pre-C/C genes. The amplified products were cloned, and 8 to 10 independent clones were sequenced. In 1983 and 1985 only one type of HBV DNA molecule was observed. Nucleotide divergence relative to the adw2 subtype was 4.7, 7.2, and 1.6%, for the pre-S1, pre-S2, and S regions, respectively, and 2.2 and 3.9% for the pre-C and C regions, respectively. In 1988 and 1989, HBV DNA forms with marked rearrangements of both the pre-S/S and pre-C/C regions were evidenced. In the pre-S/S region, they comprised two distinct HBV DNA molecules. The first showed nucleotide divergence of 20.4, 14.8, and 3.3% for the pre-S1, pre-S2, and S regions when compared with the adw2 sequence. In addition, nucleotide deletions in the pre-S1 region led to the appearance of a stop codon. The second was created by recombination between the original and mutated HBV DNA. In the pre-C/C region, the mutated viral DNA showed 11.7% divergence when compared with the adw2 sequence. A point mutation led to the creation of a stop codon in the pre-C region, together with an insertion of 36 nucleic acids in the core gene. Most of this DNA insertion was identical to that reported in an independent HBV isolate but showed no significant homology with known sequences. Semiquantitative estimation of the proportion of wild-type and mutated HBV DNA molecules showed a marked increase in the mutated forms during the period of follow-up. Sucrose gradient analysis indicated that the defective HBV DNA molecules were present in circulating virions. Western immunoblot analysis showed the appearance of modified translation products. Our findings thus indicate the emergence of and gradual takeover by mutated HBV DNA forms during the HBV chronic carrier state. The rearrangements we observed in the pre-S/S and pre-C/C genes might lead to changes in the immunogenicity of the viral particles and thus affect the clearance of the virus by the immune system.

Amino Acid Sequence↗

PubMed2003

[An efficient approach to the synthesis of a high-quality random peptide repertoire].

During the construction of a random peptide repertoire using degenerate models, unexpected amino acids or stop codons are almost unavoidable. To conquer this shortcoming, a new split-mix-split method of oligonucleotide synthesis was developed. A 13-amino acids random peptide library had been constructed by using this method. The sequencing results of 16 clones indicated that neither stop codon nor codon for cysteine appeared as designed. The occurrence rations of 19 amino acids were also calculated and no obvious amino acid bias had been observed. By using this method, the type and quantity of amino acid at certain position of a peptide could be controlled well, so this split-mix-split method, combined with degenerate could meet the needs of a high diversity random peptide library.

Amino Acid Sequence↗

PubMed1999

Translation in Bacillus subtilis: roles and trends of initiation and termination, insights from a genome analysis.

We analysed the Bacillus subtilis protein coding sequences termini, and compared it to other genomes. The analysis focused on signals, com-positional biases of nucleotides, oligonucleotides, codons and amino acids and mRNA secondary structure. AUG is the preferred start codon in all genomes, independent of their G+C content, and seems to induce less stable mRNA structures. However, it is not conserved between homologous genes neither is it preferred in highly expressed genes. In B.subtilis the ribosome binding site is very strong. We found that downstream boxes do not seem to exist either in Escherichia coli or in B.subtilis. UAA stop codon usage is correlated with the G+C content and is strongly selected in highly expressed genes. We found less stable mRNA structures at both termini, which we related to mRNA-ribosome and mRNA-release-factor interactions. This pattern seems to impose a peculiar A-rich nucleotide and codon usage bias in these regions. Finally the analysis of all proteins from B.subtilis revealed a similar amino acid bias near both termini of proteins consisting of over-representation of hydrophilic residues. This bias near the stop codon is partially release-factor specific.

Algorithms↗

PubMed2003

Mutations in CYP11B1 gene: phenotype-genotype correlations.

11beta-hydroxylase deficiency, an autosomal recessive disorder, is the second most common cause of congenital adrenal hyperplasia. We studied four subjects with classic 11beta-hydroxylase deficiency and severe hypertension: a 46,XX affected subject from a Turkish family with severe ambiguity of the external genitalia and hypertension, and three affected 46,XY subjects from a Dominican kindred with isosexual precocious puberty and severe hypertension. The affected subjects had significantly elevated plasma 11-desoxycortisol, 11-desoxycorticosterone, Delta4-androstenedione, and testosterone. To determine the molecular genetic defects, genomic DNA was isolated from the leukocytes of affected subjects and their family members. The encoding region of the 11beta-hydroxylase gene (CYP11B1) was amplified by PCR with specific primers. Using single-stranded DNA conformational polymorphism (SSCP) and DNA sequencing, a nonsense mutation in exon 6 of CYP11B1 in the affected 46,XX subject from the Turkish family was identified, where a cytosine was substituted by a thymidine, resulting in the replacement of glutamine (CAG) by a stop codon (TAG) at amino acid position 338 (Q338X). In the three 46,XY Dominican boys, the mutation was also a nonsense mutation in exon 6 of CYP11B1, where a cytosine was substituted by a thymidine, resulting in the replacement of glutamine (CAG) by a stop codon (TAG) at amino acid position 356 (Q356X). Both mutations result in the biosynthesis of a truncated 11beta-hydroxylase protein with loss of enzymatic activity. Heterozygosity was determined in family members of both probands including parents and siblings. These results indicate that mutations of CYP11B1 in these subjects are responsible for their clinical syndromes.

Adrenal Hyperplasia, Congenital↗

PubMed2005

Characterization of four receptor cDNAs: PAC1, VPAC1, a novel PAC1 and a partial GHRH in zebrafish.

To understand the role of growth hormone-releasing hormone (GHRH) and pituitary adenylate cyclase-activating polypeptide (PACAP) and to examine the functional significance of the co-expression of GHRH and PACAP in fish, their receptors were characterized in zebrafish. Three cDNAs encoding the PAC(1) receptor, the VPAC(1) receptor, and the partial GHRH receptor were identified from zebrafish. Functional expression of the PAC(1) and VPAC(1) receptors revealed that both are potently coupled to the adenylyl cyclase pathway, but only the PAC(1) receptor is coupled to the phospholipase C pathway. Transcripts for all three receptors were widely distributed, often in an overlapping pattern in the adult zebrafish. Also, one splice variant of the partial GHRH receptor and three splice variants of the PAC(1) receptor were identified from adult zebrafish. The long GHRH receptor transcript contained a 27 amino acid insert in transmembrane domain 5 encoding a premature stop codon leading to a truncated receptor protein. For the PAC(1) receptor, two of the splice variants corresponded to the hop1 and hop2 variants characterized in mammals. The third splice variant identified from the gill encoded a novel 107 bp insert containing a premature stop codon. Therefore, PACAP and GHRH have widespread, overlapping target sites suggesting a coordinated role for these hormones in evolution.

Adenylyl Cyclases↗

PubMed1997

A copia-like retrotransposon Tgmr closely linked to the Rps1-k allele that confers race-specific resistance of soybean to Phytophthora sojae.

We have isolated and characterized Tgmr, a copia-like retrotransposon, linked tightly to the Rps1-k allele that confers race-specific resistance of soybean to the the fungal pathogen Phytophthora sojae. Southern analysis followed by PCR and sequence analyses, using primers based on sequences flanking the insertion site confirmed that the element was inserted in the neighboring region of Rps1-k but not in that of the other four Rps1 alleles. This implies that Tgmr was transposed into the Rps1-k flanking site after the divergence of Rps1 alleles. Southern analysis of a series of diverse soybean cultivars revealed a high level of polymorphism of Tgmr-related sequences. These results indicate that this low copy retroelement family could have been active in the soybean genome in the recent past. Tgmr contains long terminal repeats (LTR) and four non-overlapping open reading frames (ORF), presumably originating from mutations leading to stop codons of a single ORF. The conserved domains for gag, protease, integrase, reverse transcriptase and RNaseH are present in the internal portion of the element. However, the protease, reverse transcriptase and RNaseH of this element are non-functional due to the presence of several stop codons. Possible transactivation of Tgmr and application of this element in insertional mutagenesis for soybean are discussed.

Alleles↗

PubMed1998

Genetic analysis of mutations in seven Japanese families with type I antithrombin deficiency.

We have performed genetic analysis on seven Japanese families with type I antithrombin (AT) deficiency by the polymerase chain reaction (PCR)/direct DNA sequencing method. Five distinct mutations including two novel ones were identified in six of seven families. All subjects investigated were heterozygous for the mutations. In one family, however, no genetic abnormality was found within the analyzed DNA sequences. The identified mutations were as follows: (1) a T-to-C substitution at nucleotide position 2747, which predicts an amino acid replacement of Cys (TGT) 95 by Arg, was found in two families; (2) a 4-bp deletion (-TTTC) at nucleotide position 2647-2650, which causes frameshift and a premature stop codon at codon 80; (3) a 3-bp deletion (-CTT) within nucleotide position 5356-64, which causes deletion of a Phe at amino acid numbers 121-123; (4) a C-to-T substitution at nucleotide 5381, which induces a replacement of Arg (CGA)129 by a stop codon (TGA); (5) a C-to-T substitution at nucleotide number 2745, which causes an amino acid replacement of Ala (GCC) 94 by Val (GTC). Our results confirm that the genetic background and molecular pathogenesis of type I AT deficiency is highly heterogeneous.

Adult↗

PubMed1984

Characterization of a cDNA coding for human factor X.

A lambda gt11 cDNA library containing DNA inserts prepared from human liver mRNA has been screened with an antibody to human factor X, a plasma protein participating in the middle phase of the blood coagulation cascade. Ten positive clones were isolated from 2 X 10(6) phage and plaque purified. The cDNA in the phage containing the largest insert has been sequenced and shown to code for human factor X. This cDNA insert contained 1137 base pairs coding for a portion of the light chain of the molecule, a connecting region, the heavy chain, a stop codon, a short 3' noncoding region, and a poly(A) tail. The sequence of A-T-T-A-A-A, which functions as a potential recognition site for polyadenylylation or processing, was present in the 3' end of the coding sequence and preceded the stop codon of TGA by 1 base pair and the poly(A) tail by 14 base pairs. The amino acid sequence deduced from the cDNA indicated that factor X is synthesized as a single-chain polypeptide containing the light and heavy chains connected by an Arg-Lys-Arg tripeptide. The single-chain molecule is then converted to the light and heavy chains by cleavage of two (or more) internal peptide bonds. In plasma, these two chains are linked together by a disulfide bond. The DNA sequence coding for the active site of human factor X showed a high degree of identity with prothrombin and factor IX, two other vitamin K-dependent serine proteases that participate in blood coagulation. These data along with the protein sequence data previously published for the light chain of human factor X establish the complete amino acid sequence for the mature protein present in plasma.

Amino Acid Sequence↗

PubMed2005

NKp30 (NCR3) is a pseudogene in 12 inbred and wild mouse strains, but an expressed gene in Mus caroli.

Ancient duplications and rearrangements of protein-coding segments have resulted in complex gene family relationships. As a result, gene products may acquire new specificities, altered recognition properties, modified functions, and even loss of functionality. The natural cytotoxicity receptor (NCR) family are natural killer (NK)-activating receptors whose members are NKp46 (NCR1), NKp44 (NCR2), and NKp30 (NCR3). The NCR proteins are putative immunoglobulin superfamily members whose ligands are unknown. The NKp46 gene is present and expressed in human and mouse, NKp44 is only present and expressed in human, and NKp30 is present and expressed in human but is a nonexpressed pseudogene in mouse. By searching databases we have detected alternatively spliced forms of the three NCR members. In addition, we have shown by reverse transcription-polymerase chain reaction (RT-PCR) analysis that the human NKp30 gene presents differential expression patterns in tissues. However, no expressed sequence tags (ESTs) are detected for mouse NKp30, and the genomic sequence contains two premature stop codons, which would encode a severely truncated nonfunctional protein. We have sequenced genomic DNA from 13 mouse inbred and wild strains and discovered that NKp30 is a pseudogene in every mouse strain sequenced except Mus caroli where two single nucleotide polymorphisms (SNPs) abolished the premature stop codons. We observed that the laboratory-inbred strains are, for the exonic sequences, genetically identical, except Mus m. musculus C3H. The Mus musculus strains only have a few SNPs, but the rest of the Mus strains have accumulated gradually several SNPs, mainly in the functional immunoglobulin and intracellular domains. RT-PCR analysis performed on RNA from M. caroli tissue samples identified two transcripts, one of which would encode a putative soluble NKp30 protein, also detected in rat but not in human. We have observed that the intracellular domains of NKp30 (and NKp46) are not conserved among the different species, with the most striking difference when comparing human against mouse and rat. The NKp44 gene is only found in human and shows three different splice forms varying in their "stalk" and intracellular domains. Searching for NKp44 orthologs, we found similarity to ESTs from a novel rodent TREM family member, which we termed TREM6, and not to any possible NKp44 ortholog.

Alternative Splicing↗

PubMed2006

A second independent resistance mechanism to Bacillus sphaericus binary toxin targets its alpha-glucosidase receptor in Culex quinquefasciatus.

The entomopathogen Bacillus sphaericus is an important tool for the vector control of Culex sp., and its effectiveness has been validated in field trials. The appearance of resistance to this bacterium, however, remains a threat to its use, and attempts have been made to understand the resistance mechanisms. Previous work showed that the resistance to B. sphaericus in a Culex quinquefasciatus colony is associated with the absence of the approximately 60-kDa binary toxin receptor in larvae midgut microvilli. Here, the gene encoding the C. quinquefasciatus toxin receptor, Cqm1, was cloned and sequenced from a susceptible colony. The deduced amino-acid sequence confirmed its identity as an alpha-glucosidase, and analysis of the corresponding gene sequence from resistant larvae implicated a 19-nucleotide deletion as the basis for resistance. This deletion changes the ORF and originates a premature stop codon, which prevents the synthesis of the full-length Cqm1. Expression of the truncated protein, however, was not detected when whole larvae extracts were probed with antibodies raised against an N-terminal 45-kDa recombinant fragment of Cqm1. It seems that the premature stop codon directs the mutated cqm1 to the nonsense-mediated decay pathway of mRNA degradation. In-gel assays confirmed that a single alpha-glucosidase protein is missing from the resistant colony. Further in vitro affinity assays showed that the recombinant fragment binds to the toxin, and mapped the binding site to the N-terminus of the receptor.

Amino Acid Sequence↗

PubMed2000

Molecular characterization of Mycoplasma arthritidis membrane lipoprotein MAA1.

Genes encoding the Mycoplasma arthritidis surface-exposed lipoprotein MAA1 were cloned and sequenced from MAA1-expressing strains 158p10p9 and PG6, from a low-adherence (LA) variant derived from 158p10p9 that expresses a truncated version of MAA1 (MAA1Delta) and from two MAA1-negative strains, 158 and H39. The deduced amino acid sequences of maa1 from 158p10p9 and PG6 predicted, respectively, 86.5- and 86.4-kDa basic, largely hydrophilic lipoproteins with 29-amino-acid signal peptides and predicted cleavage sites for signal peptidase II (Ala-Ala-Ala downward arrowCys). The truncation in the LA variant resulted from a G-->T substitution at nucleotide 695, which created a premature stop codon. This, in turn, generated a predicted 26.6-kDa prolipoprotein (23.6 kDa after processing), consistent with an M(r) of approximately 24,000 calculated for MAA1Delta. Similarly, absence of MAA1 expression in H39 and 158 resulted from C-->A substitutions at nucleotide 208, generating premature stop codons at that site in both strains.

Amino Acid Sequence↗

PubMed2006

Novel mutations in the respiratory syncytial virus G gene identified in viral isolates from a girl with severe combined immune deficiency treated with intravenous immune globulin.

BACKGROUND: Respiratory syncytial virus (RSV) can cause prolonged infections in individuals with compromised immunity. OBJECTIVES: To investigate whether RSV evolves during prolonged infection in an immunocompromised host. STUDY DESIGN: We sequenced the envalope glycoprotein genes of RSV obtained at three time points during a 59-day period from a 4-year-old female with severe combined immune deficiency (SCID) treated with intravenous immunoglobulin (IVIG). RESULTS: Sporadic silent mutations were found in the SH, G and F genes among three RSV samples collected at days 0, 19 and 59. Premature stop codons at amino acid positions 257 and 278 were present in the RSV G glycoprotein gene sequenced from each time point. None of the 48 RSV G sequences available on GenBank or any of 50 genetically diverse clinical isolates of RSV contained these mutations. These premature stop codon mutations occurred at the same positions of the G glycoprotein gene as those described in in vitro monoclonal-antibody resistant mutants reported elsewhere. CONCLUSION: Our patient was most likely infected with a single RSV strain that did not mutate during the study period. This strain contains unique mutations that may have previously evolved in this individual who had prolonged infection and was treated with monthly IVIG.

Amino Acid Sequence↗

PubMed1996

Molecular defects in TCRBV genes preclude thymic selection and limit the expressed TCR repertoire.

A prerequisite for the assembly of a functional TCR is the rearrangement of gene segments to result in in-frame transcripts that can vary in length across the CDR3 region. Selection for in-frame 3-bp spaced rearrangements is observed for functional TCRB genes in thymocyte DNA and mRNA transcripts from PBMC. Previous analyses of the expressed human TCRBV gene repertoire have suggested that BV10S1 and BV19S1 gene segments may be expressed at very low levels or not at all in some individuals. CDR3 size analysis for BV10 and BV19 transcripts and thymic DNA rearrangements revealed no such selection of in-frame 3-bp spaced rearrangements. Comparison of the BV19 leader intron sequence with consensus 5'-splice signal sequences suggested that the mature mRNA for this gene would contain the unspliced leader intron. Sequencing of BV19 transcripts from PBMC confirmed that the intron was not spliced, resulting in a predicted translation product that terminates prematurely. Both genomic DNA and mRNA were analyzed for the BV10 gene. The leader sequence contained a single extra base, which would result in a shift in the V region reading frame upon conventional mRNA splicing. This gene is predicted to be nonfunctional due to the presence of a stop codon in the V gene segment just after the splice signal. A splice variant that uses an alternative 3'-splice site further downstream in the V region was also detected. This variant is predicted to be nonfunctional due to the presence of an in-frame stop codon in the V region. These processing defects are sufficient to abrogate positive selection. Therefore, the conclusions drawn from previous studies of the expressed T cell repertoire in normal and disease states based on the presumed functional status of these two genes need to be reassessed.

Base Sequence↗

PubMed1994

A frame-specific symmetry of complementary strands of DNA suggests the existence of genes on the antisense strand.

The bacterial DNA sequence in GenBank database were divided into coding and noncoding regions and examined for the base-trimer distribution in every triplet frame on the sense and antisense strands. The results revealed that for the noncoding region, both strands have very similar base-trimer distributions and have no frame specificity; that is, DNA is symmetric in the noncoding region. For the coding region, on the other hand, the symmetry is broken only in the triplet framework, and we found a special triplet-frame-specific symmetry which appears when the two complementary strands of the coding region are read from their 5' ends. In addition, the following frame specificity was also observed in the distribution of stop codons on the antisense strand of the coding region. When the antisense sequences of the open reading frames (ORFs) in the database are read in the three reading frames, the same reading frame as the corresponding ORF contains a significantly larger amount of long open frames without stop codons (i.e., nonstop frames [NSFs]) than expected, while the number of NSFs in the other two reading frames is similar to that of the expected one. That is, NSFs as well as ORFs are maintained in a frame-specific manner, and in this sense, DNA becomes symmetrical even in the coding region. These two kinds of frame-specific symmetries indicate that only an ORF and its complementary triplets are specifically recognized and maintained in DNA.(ABSTRACT TRUNCATED AT 250 WORDS)

DNA, Antisense↗

PubMed1992

Loss of V protein expression in human parainfluenza virus type 1 is not a recent event.

The P gene of paramyxoviruses usually contains an alternate overlapping ORF coding for a short cysteine-rich domain called V. This domain was thought to be a common feature of these genes as it is present in ten paramyxoviruses. However, the V ORF region of the P gene of one strain of human parainfluenza-virus type 1 (isolated in 1957) was recently found to be closed by no less than 9 stop codons. To determine whether the absence of the V ORF here might be due to the long adaptation of this strain in culture, 3 other more recent isolates were examined. Small differences in the V region were found, but all had conserved the vast majority of the stop codons. Moreover, examination of most of the intercistronic regions of the PIV1 genome failed to uncover a cryptic V gene. The V ORF is then unlikely to be a common feature of paramyxovirus P genes.

Amino Acid Sequence↗