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PubMed2001

Molecular epidemiology of viral pathogens and tracing of transmission routes: hepatitis-, calici- and hantaviruses.

BACKGROUND: The need to rapidly identify new therapeutic drugs and vaccines for clinically important viral infections has resulted in intensive study of the molecular properties of viruses. Modern molecular techniques have provided tools for tracing infections and studying the evolution of viruses. OBJECTIVE STUDY AND DESIGN: Two examples illustrating how modern molecular techniques can be used in clinical virology and molecular epidemiology (hepatitis and caliciviruses), and one example documenting their importance in basic research (hantaviruses) will be discussed. RESULTS AND CONCLUSIONS: Water- and food-borne outbreaks caused by the faeco-orally spread hepatitis A virus (HAV) are common in areas lacking proper sanitation, but they are possible also in countries with low seroprevalence. In water epidemics, the sequence comparisons between the virus from patients and from water have been used successfully. Hepatitis B virus variants are clinically important and challenge the diagnostic tests and prophylactic measures. Some hepatitis C (HCV) genotypes appear to be associated with more severe pathology and others respond better to antiviral treatment. Nosocomial and occupational infections are not rare, and the source can be identified by phylogenetic analysis of nucleotide sequences obtained from the infected individuals. The overwhelming role of Norwalk-like caliciviruses (NLV) in adult diarrhoea and especially in food- and water-borne epidemics has become apparent during the last decade. Methods are under development for detecting these viruses, not only from patient samples and water, but also from other environmental samples (e.g. foodstuff and surface swabs). The analysis of the genetic variation and evolution of the Old World hantaviruses in their carrier rodents has shown that the extent of genetic diversity correlates with geographical distance. As a rule, phylogenetic relationships of hantaviruses resemble those of their rodent hosts, suggesting virus-host co-evolution. Exceptional host-switch events allow a study on still radiating hantavirus species. There is suggestive evidence that natural reassortant hantaviruses are involved in human infection.

Animals↗
PubMedDate not supplied

Primate hepatitis B viruses - genetic diversity, geography and evolution.

There are six well characterised genotypes (A-F) of human hepatitis B virus that have distinct geographic ranges which generally relate to chronic HBV infection. A seventh human genotype (G) has recently been described, but there is limited information on ethnic and geographic distribution. Despite the fact that early studies indicated that HBV antigens were present in other primates, the prevailing dogma that HBV was a human disease precluded alternative explanations. Within the past 5 years, hepatitis B viruses have been characterised from all the Old World great apes (orangutan, gibbons, gorillas and chimpanzees) and from a New World woolly monkey. Each group of non-human primates appears to have a distinct strain of hepatitis B virus that can be distinguished from human sequences based upon the nucleotide sequence and selected amino acid changes in the viral proteins. The woolly monkey HBV is most divergent from other primate and human sequences, while the great ape HBV sequences cluster together with separate branches for each group.

Animals↗
PubMed2004

Complete DNA sequence analyses of the first two varicella-zoster virus glycoprotein E (D150N) mutant viruses found in North America: evolution of genotypes with an accelerated cell spread phenotype.

Varicella-zoster virus (VZV) is considered to be one of the most genetically stable of all the herpesviruses. Yet two VZV strains with a D150N missense mutation within the gE glycoprotein were isolated in North America in 1998 and 2002. The mutant strains have an accelerated cell spread phenotype, which distinguishes them from all wild-type and laboratory viruses. Since the VZV genome contains 70 additional open reading frames (ORFs), the possibility existed that the phenotypic change was actually due to an as-yet-undiscovered mutation or deletion elsewhere in the genome. To exclude this hypothesis, the entire genomes of the two mutant viruses were sequenced and found to contain 124,883 (VZV-MSP) and 125,459 (VZV-BC) nucleotides. Coding single-nucleotide polymorphisms (SNPs) were identified in 14 ORFs. One missense mutation was discovered in gH, but none was found in gB, gI, gL, or gK. There were no coding SNPs in the major regulatory protein ORF 62. One polymorphism was discovered which could never have been anticipated based on current knowledge of herpesvirus genomics, namely, the origins of replication differed from those in the prototype strain but not in a manner expected to affect cell spread. When the two complete mutant VZV sequences were surveyed in their entirety, the most reasonable conclusion was that the increased cell spread phenotype was dependent substantially or solely on the single D150N polymorphism in glycoprotein gE. The genomic results also expanded the evolutionary database by identifying which VZV ORFs were more likely to mutate over time.

Aged↗
PubMed2002

Observation of positive selection within hypervariable regions of a newly identified DNA virus (SEN virus)(1).

To elucidate the evolution of SEN virus (SEN-V), serial sequences of chronically SEN-V-infected patients were analyzed. In the hypervariable regions, non-synonymous substitutions significantly predominated. This could be attributed to positive selection in evading immune surveillance of the hosts and to establish a persistent infection. On the basis of the sequences in the two open reading frames of SEN-V DNA, the rate of synonymous substitutions was 7.32 x 10(-4) per site per year. Since this rate is close to RNA viruses and higher than other DNA viruses, the SEN-V might be replicated by machinery with poor or no proofreading function.

Chronic Disease↗
PubMed1997

[Follow-up serological study of herpes simplex and cytomegalovirus in Cuban patients infected with human immunodeficiency virus (HIV)].

The evolution serological response against the herpes simplex virus and citomegalovirus in HIV infected patients grouped into different stages of the disease was studied. Fluctuations in the TPG of antibodies were observed in these values in a cyclical way through time. There was a greater significant difference among the TPG of antibodies against HSV in the group of asymptomatic patients compared with AIDS patients and with those who died. There is a marked decrease in the TPG of antibodies against HSV and CMV approximately one year before the death of patients.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Pathways of evolution of influenza A (H1N1) viruses from 1977 to 1986 as determined by oligonucleotide mapping and sequencing studies.

The evolutionary relationships of epidemic influenza A (H1N1) viruses isolated between 1982 and 1986 have been examined by oligonucleotide mapping and partial DNA sequencing. The T1 mapping studies confirmed our previous report that the evolution of the influenza virus genome generally results in an average of four to six oligonucleotide changes per year. Between 1982 and 1986, however, two apparent exceptions to this finding occurred. H1N1 antigenic variants (including the A/Chile/83 and A/Victoria/83 reference strains) that caused influenza outbreaks and epidemics from 1983 to 1984 differed by 20 to 30 oligonucleotides from viruses isolated during the previous influenza season. T1 mapping of individual RNA segments and sequencing revealed that all six internal genes of a representative 1983 A/Chile-like virus were more closely related to genes of non-reassortant H1N1 viruses that circulated from 1977 to 1982 than to genes of H3N2 viruses. Therefore, the 1983 variant viruses were not H1N1-H3N2 reassortants. The A/Taiwan/86-like H1N1 antigenic variants that emerged in south-east Asia in the spring of 1986 and caused epidemic activity the following winter also exhibited changes of 20 to 30 oligonucleotides from the A/Chile/83-like or A/Victoria/83-like H1N1 viruses that circulated during the previous influenza season. Fewer oligonucleotide changes were observed between the 1986 A/Taiwan/86-like and H1N1 viruses isolated before 1983, however, suggesting that the former evolved from viruses that circulated before the 1983 antigenic variants became the predominant H1N1 epidemic virus strains. This was confirmed by sequencing the HA1 domain of the haemagglutinin genes of three A/Taiwan/86-like viruses. These studies provide evidence that other genes of influenza A viruses, in addition to the haemagglutinin gene, may evolve concurrently along two or more separate pathways.

Amino Acid Sequence↗
PubMed2004

Evolution of the HIV-1 envelope glycoproteins with a disulfide bond between gp120 and gp41.

BACKGROUND: We previously described the construction of an HIV-1 envelope glycoprotein complex (Env) that is stabilized by an engineered intermolecular disulfide bond (SOS) between gp120 and gp41. The modified Env protein antigenically mimics the functional wild-type Env complex. Here, we explore the effects of the covalent gp120 - gp41 interaction on virus replication and evolution. RESULTS: An HIV-1 molecular clone containing the SOS Env gene was only minimally replication competent, suggesting that the engineered disulfide bond substantially impaired Env function. However, virus evolution occurred in cell culture infections, and it eventually always led to elimination of the intermolecular disulfide bond. In the course of these evolution studies, we identified additional and unusual second-site reversions within gp41. CONCLUSIONS: These evolution paths highlight residues that play an important role in the interaction between gp120 and gp41. Furthermore, our results suggest that a covalent gp120 - gp41 interaction is incompatible with HIV-1 Env function, probably because this impedes conformational changes that are necessary for fusion to occur, which may involve the complete dissociation of gp120 from gp41.

Amino Acid Substitution↗
PubMed2003

A longitudinal assessment of autologous neutralizing antibodies in children perinatally infected with human immunodeficiency virus type 1.

The evolution of autologous neutralizing antibodies to sequential human immunodeficiency virus type 1 (HIV-1) isolates was studied in a population of 16 children who were perinatally infected with human immunodeficiency virus type 1. The cohort included seven children with rapid disease progression (RP) and nine who had nonrapid disease progression (NRP). Four of the NRP after 6 months of age harbored viruses that could be neutralized by antibodies found in autologous contemporaneous plasma (titers up to 1:640) while the majority of longitudinally collected viruses from five NRP were resistant to neutralization with contemporaneous plasma. Because of their shorter survival, only five of the RP had studies after 6 months of age; three of the five had neutralizing antibodies to contemporaneous virus isolates and the highest titers were 1:20. The highest titers in RP (up to 1:160) occurred in specimens obtained prior to 6 months of age but these were most likely of maternal origin. Most isolates that were not neutralized by contemporaneous plasma could be neutralized using noncontemporaneous plasma obtained months to years after the virus isolates. These autologous noncontemporaneous neutralizing antibodies persisted for years, had titers that were higher to viruses isolated at younger ages, and were generally more potent in children with NRP than RP. Demonstration of neutralizing antibodies to viruses previously resistant to neutralization by contemporaneous plasma suggests a continuous evolution of virus variants in vivo that are able to escape the effect of neutralizing antibodies.

Antibody Specificity↗
PubMed1985

Viruses in fungi and eukaryotic algae: their possible origins and evolution.

It now seems that isometric viruses isolated from higher fungi contain double-stranded RNA whereas those from the primitive lower fungi and eukaryotic algae possess double-stranded DNA. The possible origins and evolution of the viruses are discussed on the basis of their biological and morphological features.

Biological Evolution↗
PubMed1996

Adaptive evolution of human immunodeficiency virus-type 1 during the natural course of infection.

The rate of progression to disease varies considerably among individuals infected with human immunodeficiency virus-type 1 (HIV-1). Analyses of semiannual blood samples obtained from six infected men showed that a rapid rate of CD4 T cell loss was associated with relative evolutionary stasis of the HIV-1 quasispecies virus population. More moderate rates of CD4 T cell loss correlated with genetic evolution within three of four subjects. Consistent with selection by the immune constraints of these subjects, amino acid changes were apparent within the appropriate epitopes of human leukocyte antigen class I-restricted cytotoxic T lymphocytes. Thus, the evolutionary dynamics exhibited by the HIV-1 quasispecies virus populations under natural selection are compatible with adaptive evolution.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Novel and dynamic evolution of equine infectious anemia virus genomic quasispecies associated with sequential disease cycles in an experimentally infected pony.

We have investigated the genetic evolution of three functionally distinct regions of the equine infectious anemia virus (EIAV) genome (env, rev, and long terminal repeat) during recurring febrile episodes in a pony experimentally infected with a well-characterized reference biological clone designated EIAV(PV). Viral populations present in the plasma of an EIAV(PV)-infected pony during sequential febrile episodes (18, 34, 80, 106, and 337 days postinfection) were amplified from viral RNA, analyzed, and compared to the inoculated strain. The comparison of the viral quasispecies showed that the inoculated EIAV(PV) quasispecies were all represented during the first febrile episode, but entirely replaced at the time of the second febrile episode, and that new predominant quasispecies were associated with each subsequent cycle of disease. One of the more surprising results was the in vivo generation of large deletion (up to 15 amino acids) in the principal neutralizing domain (PND) of gp90 during the third febrile episode. This deletion did not alter the competence for in vitro replication as shown by the analysis of a env chimeric clone with a partially deleted PND and did not altered the fitness of the virus in vivo, since this partially deleted envelope became the major population during the fourth febrile episode. Finally, we showed that the amino acid mutations were not randomly distributed but delineated eight variables regions, V1 to V8, with V3 containing the PND region. These studies provide the first detailed description of the evolution of EIAV genomic quasispecies during persistent infection and reveal new insights into the genetics and potential mechanisms of lentivirus genomic variation.

Amino Acid Sequence↗
PubMed1991

Levels of selection, evolution of sex in RNA viruses, and the origin of life.

Multi-component RNA viruses have genomes that are segmented into two or more RNA molecules. A viral particle carries only one RNA molecule. Reproduction of a particle requires complementation by particles carrying other segments of the genome. Complementation is achieved when a group of particles co-infects the same host cell and forms a co-infection group. I have previously proposed the hypothesis that multi-component reproduction evolved in RNA viruses as a form of sex. Multi-component viruses may need sex because, like all RNA viruses, they have very high mutation rates. On the other hand, Nee (1987, J. molec. Biol. 25, 277-281.) has proposed the hypothesis that multi-component genomes evolved because smaller RNA molecules are favored by selection on RNAs within a host cell. Nee (1989, J. theor. Biol. 138, 407-412.) also claimed that selection on RNAs alone can account for the evolution of multi-component viruses. He criticized the viral sex hypothesis because, in his view, co-infection groups are not units of selection and are too transient to be engaged in sex. These two hypotheses were further examined through population genetic models. Three evolutionary agents are assumed to operate in the models. Selection on co-infection groups favors retention of the genome on one large RNA molecule because larger RNAs require less complementation. Selection on RNAs favor segmentation of the viral genome into smaller RNAs, which are replicated and encapsidated more rapidly. Mutation pressure also favors smaller molecules because those molecules are smaller targets for deleterious mutations. Analysis of the models shows that (when parameter values argued to be biologically realistic are used) selection on co-infection groups is necessary for the evolutionary persistence of multi-component viruses. Without selection on co-infections groups to oppose mutation pressure and selection on RNAs, a population of multi-component viruses is displaced by a population of parasitic viral RNAs that are replication and encapsidation specialists. These results support arguments that co-infection groups are units of selection in multi-component viruses. Both mutation pressure and selection on RNAs may be responsible for the evolution of genome segmentation in multi-component viruses because there is good evidence documenting the action of both in RNA viruses.(ABSTRACT TRUNCATED AT 400 WORDS)

Biological Evolution↗
PubMed1991

Small cysteine-rich proteins of different groups of plant RNA viruses are related to different families of nucleic acid-binding proteins.

The 3'-terminal genes in genomic RNAs of four groups of plant positive strand RNA viruses (hordei-, furo-, tobra-, and carlaviruses) encode small proteins enriched in Cys residues. The arrangement of Cys and in some cases also His residues in these proteins is compatible with finger formation. A computer-assisted sequence comparison of viral Cys-rich proteins reveals no significant similarity between them. It is shown that the hordeivirus Cys-rich protein (17K) is related to a group of chloroplast tRNA intron-encoded proteins, whereas the respective furovirus protein (14K) is similar to E6 proteins of papillomaviruses. Somewhat less significant similarity, marked, however, by conservation of a number of positively charged residues, was observed between the sequences of tobravirus Cys-rich proteins and the basic domains of high mobility group chromatin proteins. It can be speculated that plant RNA virus Cys-rich proteins bind RNA and/or DNA and might be involved in regulation of virus and/or host genome expression. In the course of evolution these virus proteins may have originated from different nucleic acid-binding proteins.

Amino Acid Sequence↗
PubMed2002

Cell turnover and cell tropism in HIV-1 infection.

Early infection with HIV-1 is dominated by CCR5-tropic (R5, non-syncytium-inducing) viruses. The evolution of CXCR4-tropic (X4, syncytium-inducing) viruses occurs later in the infection and is associated with rapid disease progression. Here, we propose that the tropism of X4 viruses for naive CD4+ T cells is disadvantageous in early infection owing to the low division rate of these cells. In healthy individuals, the division rate of memory cells is nearly ten times higher than that of naive cells and thus the memory-cell tropism of R5 viruses could account for their dominance early in infection. As the division rate of naive T cells increases with CD4+ depletion, X4 viruses come to dominate in late disease.

CD4-Positive T-Lymphocytes↗
PubMed1989

Is HIV unique or merely different?

The HIV epidemic is similar to previous human epidemics, and our early responses to the HIV epidemic have likewise been similar. Furthermore, HIV is similar to other single-stranded RNA viruses in its evolution. Like other RNA viruses, HIV has a high mutation rate and thus evolves rapidly. This rapid evolution may make it difficult to develop a successful vaccine against HIV, and perhaps may also limit the usefulness of drugs because of the appearance of resistant mutants. However, most of the variation in HIV nucleotide sequences is neutral, not adaptive. Other viruses in the same retrovirus subfamily as HIV (lentiviruses) are also successful pathogens in animals and are difficult to control without the added problem of the social factors that exist for HIV. These social factors involved in HIV transmission make HIV hard to control by usual public health measures. The prevalence of syphilis and hepatitis B in the United States shows that neither a successful drug treatment nor an effective vaccine is sufficient to stop some infectious diseases when social factors are involved. For these reasons, I conclude that the HIV/AIDs epidemic is different, but not unique.

Acquired Immunodeficiency Syndrome↗