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PubMed1990

Generation and transmission of Rift Valley fever viral reassortants by the mosquito Culex pipiens.

Reassortant viruses containing heterologous S and M genomic RNA segments were obtained from both mosquito and vertebrate hosts that had been coinfected with Egyptian and Senegalese strains of Rift Valley fever (RVF) virus. The origin of the S and M RNA segments in each plaque-cloned virus was determined with monoclonal antibodies capable of differentiating the nucleocapsid protein (S segment marker) or the G1 glycoprotein (M segment marker) of the parental strains. In the mosquito Culex pipiens, reassortants were detected after sequential ingestion of parental viruses by interrupted feeding on two infected hamster hosts, after feeding on a single host that had been infected with both parental strains, and from individual mosquitoes inoculated intrathoracically with both parental strains. Reassortant viruses replicated efficiently in mosquitoes and were readily transmissible by bite to hamsters. Replication of a second infecting strain of RVF virus was, however, completely inhibited if that virus was inoculated into a mosquito greater than or equal to 48 h after the first viral strain. Genetic reassortment may provide a mechanism for increased heterogeneity, and thus affect the epidemiology and evolution of RVF virus.

Animals↗

PubMed1977

The control of influenza.

Influenza virus differs from the usual agents of epidemic disease by its extreme variability. Since consecutive outbreaks are caused by antigenically different viruses, both herd immunity and vaccination are largely ineffective and the epidemiology is characterized by pandemics, sensu stricto. Severe pandemics occur every 10-12 years, followed by a period (subtype era) over which the evolution of the virus follows a predictably regular course. This process can be imitated in the laboratory, yielding mutant viruses which may serve as prospective vaccines. The transition between subtypes is abrupt and hitherto unpredictable. There are indications, however, that the number of subtypes is limited and that they are linked in a secular cycle of about 70 years. If this proves to be correct, it should be possible to anticipate even the major antigenic shifts and thus eventually fully control the disease.

Antibody Formation↗

PubMed2002

Frequency-dependent selection in human immunodeficiency virus type 1.

Genetic variation is the main evolutionary strategy adopted by RNA viruses and retroviruses. Evolution operates through competition between different individuals in the same environment, resulting in the imposition of the fittest variant. The process of competition could be affected by various factors, including the frequency of the different competing individuals. In order to investigate this aspect, individual virus populations derived from a human immunodeficiency virus type 1 isolate were studied at different competing proportions. The dynamics of variant imposition in each competition experiment permitted the detection of frequency-dependent selection (FDS); i.e. the imposition of variants is related to their biological fitness, which is also affected by the proportions at which they compete. The existence of FDS in different viruses with RNA genomes would indicate a general mechanism favouring genetic heterogeneity.

Adaptation, Physiological↗

PubMed1987

Hepatocarcinogenicity of the woodchuck hepatitis virus.

During investigations of the evolution of experimental laboratory infections of woodchucks (Marmota monax) with the woodchuck hepatitis virus (WHV), eight hepatocellular carcinomas (HCC) were observed, six in newborns and two in young adult animals, all within 17-36 months after infection. The absence of an external cocarcinogenic effect in the well-monitored woodchucks indicates the carcinogenicity of WHV and suggests the same for the genetically and biologically similar human hepatitis B virus (HBV). Laboratory infections of woodchucks with two strains of WHV, not reported here in detail, resembled human and chimpanzee HBV infections histologically and serologically. In these studies, eight woodchucks became carriers of surface antigen of WHV for greater than 1 year. All eight woodchucks developed HCC, indicating a 100% risk of HCC in experimentally infected chronic WHV antigen carriers, which is analogous to the high risk of HCC in human hepatitis B surface antigen carriers. Histologically, the absence of cirrhosis in the examined pericarcinomatous tissue permits recognition of gradual transition from normal parenchyma to neoplastic nodules to HCC of rising anaplasia, indicating a continuum of increasingly more malignant neoplastic stages, as known for chemical carcinogenesis. The HCC developed in carrier woodchucks infected as newborns with only minor, if any, hepatitic changes but is associated with antigen-carrying hepatocytes and sometimes with hyperplastic nodules. This stage was preceded in infected adults by an early, acute, weeks-long hepatitis coinciding with the appearance of surface antigen. These findings are also analogous to typical HBV infection in human newborns and young adults, respectively. At the time of HCC development in all animals with adequate histologic material, an acute recent necroinflammation appeared around the tumor, associated with abnormal hematopoietic cells around and within the tumor. A promoting role in carcinogenesis of this necroinflammation of yet unestablished pathogenesis is being postulated, to be confirmed by determination of the status of the WHV DNA in the HCC and by prospective histologic study of the inflammatory reaction.

Animals↗

PubMed1998

An African HIV-1 sequence from 1959 and implications for the origin of the epidemic.

There is considerable genetic diversity among viruses of different subtypes (designated A to J) in the major group of human immunodeficiency virus type 1 (HIV-1), the form of HIV that is dominant in the global epidemic. If available, HIV-1 sequences pre-dating the recognition of AIDS could be crucial in defining the time of origin and the subsequent evolution of these viruses in humans. The oldest known case of HIV-1 infection was reported to be that of a sailor from Manchester who died of an AIDS-like illness in 1959; however, the authenticity of this case has not been confirmed. Genetic analysis of sequences from clinical materials obtained from 1971 to 1976 from members of a Norwegian family infected earlier than 1971 showed that they carried viruses of the HIV-1 outlier group, a variant form that is mainly restricted to West Africa. Here we report the amplification and characterization of viral sequences from a 1959 African plasma sample that was previously found to be HIV-1 seropositive. Multiple phylogenetic analyses not only authenticate this case as the oldest known HIV-1 infection, but also place its viral sequence near the ancestral node of subtypes B and D in the major group, indicating that these HIV-1 subtypes, and perhaps all major-group viruses, may have evolved from a single introduction into the African population not long before 1959.

Democratic Republic of the Congo↗

PubMed1996

Geographical distribution of the human polyomavirus JC virus type A and B and isolation of a new type from Ghana.

The JC polyomavirus (JCV) is ubiquitous in humans infecting children asymptomatically, then persisting in renal tissue. Since JCV DNA can be readily isolated from urine, it should be a useful tool with which to study the evolution of DNA viruses in humans. We showed that JCV DNA from the urine of Japanese, Taiwanese, Dutch and German patients can be classified into A and B types, based upon restriction fragment length polymorphisms (RFLPs). This work was extended in the present study. We established multiple JCV DNA clones from the UK, Spain, Italy, Sweden, South Korea, People's Republic of China, Malaysia, Indonesia, Mongolia, India, Sri Lanka, Saudi Arabia, Ethiopia, Kenya, Zambia, South Africa and Ghana. Using type-specific RFLPs, most clones except the four clones from Ghana were classified as either type A or B. We constructed a molecular phylogenetic tree for the Ghanaian clones and several representative type A and B clones. According to the phylogenetic tree, the Ghanaian clones constituted a major new group, tentatively named type C. From the findings presented here and elsewhere, the following conclusions were drawn: (i) type A is prevalent only in Europe; (ii) type B is found mainly in Asia and Africa; and (iii) type C is localized to part of Africa. Our findings should help to clarify how JCV evolved in humans.

Base Sequence↗

PubMed2005

Molecular analysis of the NS3/NS3A gene of Bluetongue virus isolates from the 1979 and 1998-2001 epizootics in Greece and their segregation into two distinct groups.

The sequence of the genome segment 10 (Seg-10) encoding NS3/NS3A was determined for 19 field isolates of Bluetongue virus (BTV) of serotypes BTV-1, BTV-4, BTV-9 and BTV-16, derived from epizootics in Greece in the years 1979 and 1998-2001. The aim of the study was to define the molecular epidemiology of the virus in this part of the Mediterranean basin. On the basis of the Seg-10 sequences, the isolates grouped into two distinct phylogenetic clusters. These were Greek group I of solely serotype BTV-4 viruses, and Greek group II of serotypes BTV-1, BTV-9 and BTV-16 viruses. The isolates in Greek group I clustered with the Corsican and Tunisian BTV-2 serotypes and US group II strains of BTV-10 and BTV-13 serotypes, while those in Greek group II with Chinese, Indian and Australian viruses of different serotypes suggesting that viruses derived from two distinct ecosystems have caused BT incursions in Greece over the last 25 years. The NS3/NS3A sequences of most of the BTV-4 isolates were identical, irrespective of the year of isolation, geographical location and host species or tissue origin. Maximum of 15-16% nucleic acid sequence variation, but only 4% deduced amino acid substitution, were observed between groups I and II. Furthermore, the clustering of the NS3/NS3A sequences was independent of the viral serotype, indicating the occurrence of genome segment reassortment during the course of evolution of the viruses.

Amino Acid Sequence↗

PubMed1977

Purification and biochemical properties of Egtved viral RNA.

32P-labeled Egtved virus RNA was released from highly purified virus by phenol-SDS extraction. The single-stranded nature of the RNA was demonstrated by (1) its buoyant density of 1.69 g/cm3 in Cs2-SO4, (2) its susceptibility to digestion by pancreatic ribonuclease in either 1 X SSC or 0.01 X SSC (standard saline citrate), (3) its base composition (29.3% C, 23.6% A, 14.5% U. 32.6% G). This Egtved virus is different from the other rhabdoviruses since the base composition of its genomic RNA is lower in its composition of A + U. Such a result could have possible taxonomic implications concerning the orignin and evolution of Egtved Virus relative to the other known rhabdoviruses.

Adenine↗

PubMedDate not supplied

Interactions between viscerotropic velogenic Newcastle disease virus and pet birds of six species. II. Viral evolution through bird passage.

Following in vivo studies in pet birds of 6 species, 279 Newcastle disease virus (NDV) reisolates were selected for characterization by the embryonated-chicken-egg mean-death-time, plaque-assay, hemagglutination-elution, and hemagglutinin-thermostability techniques. Initially, the 279 isolates were screened by the mean-death-time and plaque-assay techniques, and 5 sequential isolates were chosen for each of 3 budgerigars and 2 parrots for characterization by the other 2 in vitro assays to determine whether the Colorado Psittacine Isolate of viscerotropic velogenic (VV) NDV (COPI-VVNDV) had evolved during passage through pet birds. Nineteen isolates were then selected for chicken back-passage studies. Fifteen of the 19 isolates were chosen for potential avirulence for 8-week-old domestic chickens. The 4 remaining isolates produced large red plaques when assayed and were therefore used as virulent virus controls likely to be VVNDV. Subsequent in vitro characterization of selected back-passage chicken NDV isolates demonstrated little change in the 4 parameters originally evaluated for the pet-bird isolates used for the back-passage studies. Although the psittacine isolate slowly evolved to relatively avirulent strains of NDV by passage in pet birds, reversion did not occur during the chicken back-passage studies.

Animals↗

PubMed2000

Evolution of lamivudine resistance in human immunodeficiency virus type 1-infected individuals: the relative roles of drift and selection.

Human immunodeficiency virus type 1 (HIV-1) rapidly develops resistance to lamivudine during monotherapy, typically resulting in the appearance at position 184 in reverse transcriptase (RT) of isoleucine instead of the wild-type methionine (M184I) early in therapy, which is later replaced by valine (M184V). M184V reduces viral susceptibility to drug in vitro by approximately 100-fold, but also results in a lower processivity of RT. We show that a drop in absolute viral fitness associated with the outgrowth of M184V results in a drop in viral load only in individuals with high CD4(+) counts, from whom we estimate the relative fitness of M184V in the presence of drug to be approximately 10% of that of the wild type prior to therapy. The timing of emergence of the M184V mutant varies widely between infected individuals. From analysis of the frequency of M184I and M184V mutants determined at multiple time points in seven individuals during lamivudine therapy, we estimated the fitness advantage of M184V over M184I during therapy to be approximately 23% on average. We have also estimated the average ratio of the frequencies of the two mutants prior to therapy to be 0. 2:1, with a range from 0.12:1 to 0.33:1. We have found that the differences between individuals in the rate of evolution of lamivudine resistance arise due to genetic drift affecting the relative frequency of M184I and M184V prior to therapy. These results show that stochastic effects can be significant in HIV evolution, even when there is large fitness difference between mutant and wild-type variants.

Anti-HIV Agents↗

PubMed2003

Influence of reverse transcriptase variants, drugs, and Vpr on human immunodeficiency virus type 1 mutant frequencies.

The evolution of drug resistance is a major complication of human immunodeficiency virus type 1 (HIV-1) chemotherapy. HIV-1 reverse transcriptase (RT) is a major target of antiretroviral therapy and ultimately the target of drug resistance mutations. Previous studies have indicated that drug-resistant HIV-1 RTs can alter HIV-1 mutant frequencies. In this study, we have tested a panel of HIV-1 RT variants for their ability to influence virus mutant frequencies. The RT variants tested included drug-resistant RT variants as well as other variants analyzed in enzyme fidelity studies with the lacZalpha gene as a mutation target and/or implicated as being important for enzyme fidelity by structural studies. Combinations of mutations that alone had a statistically significant influence on virus mutant frequencies resulted in different mutant frequency phenotypes. Furthermore, when virus replication occurred in the presence of drugs [e.g., 3'-azido-3'-deoxythymidine, (-)2/,3'-dideoxy-3'-thiacytidine, hydroxyurea, thymidine, or thioguanine] with selected RT variants, virus mutant frequencies increased. Similarly, Vpr variants deficient for binding to the uracil DNA glycosylase repair enzyme were observed to influence HIV-1 virus mutant frequencies when tested alone or in combination with RT variants. In summary, these observations indicate that HIV-1 mutant frequencies can significantly change by single amino acid substitutions in RT and that these effects can be altered by additional mutations in RT, by drugs, and/or by expression of Vpr variants. Such altered virus mutant frequencies could impact HIV-1 dynamics and evolution in small population sizes.

Amino Acid Substitution↗

PubMed1997

Correlation between antiretroviral resistance mutations, biological parameters, and clinical evolution in zidovudine-treated patients infected with human immunodeficiency virus type 1.

To evaluate the correlation between zidovudine (ZDV) resistance mutations of human immunodeficiency virus type 1 (HIV-1), biological parameters, and clinical evolution, 111 HIV-1-infected patients treated with ZDV were studied. Specific mutations at codons 70, 215, and 41 in the HIV-1 reverse transcriptase coding region conferring resistance to ZDV were detected using a selective polymerase chain reaction. The appearance of ZDV resistance mutations was significantly correlated with baseline clinical stage, CD4+ cell count, and viral load, but not with duration of ZDV therapy or p24 antigen level. In univariate analysis, results showed a prognostic role of mutations at codons 215 and 41 for clinical progression to the acquired immune deficiency syndrome (AIDS) or death. In multivariate analysis after controlling for viral load, CD4+ cell count, and clinical stage, the presence of the mutation at codon 215 (but not at codon 41) remained an independent predictor of subsequent clinical evolution.

Adult↗

PubMed2005

Interaction of the hepatitis B virus protein HBx with the human transcription regulatory protein p120E4F in vitro.

Infection with the hepatitis B virus has been identified as one of the major causes of liver cancer. A large body of experimental work points to a central role for the virally encoded protein HBx in this form of carcinogenesis. HBx is expressed in HBV-infected liver cells and interacts with a wide range of cellular proteins, thereby interfering in cellular processes including cell signaling, cycle regulation and apoptosis. In order to identify possible new targets of the HBx protein, we performed a yeast two-hybrid screen using a truncated protein mini-HBx(18-142) as the bait. In addition to known interacting partners, such as RXR and UVDDB1, we identified several new candidates including the human transcriptional regulatory protein p120E4F, which has been implicated in the regulation of mitosis and the cell cycle. In vitro pull down experiments confirmed the interaction and transcription activation assays in the yeast demonstrated that HBx protein was able to repress GAL4AD-p120E4F-dependent activation of a reporter gene under the control of E4F binding sites found in the adenovirus E4 promoter and the HBV enhancer II region. We also showed that the cysteine residues in HBx are necessary for its interaction with UVDDB1 but not for the interaction with RXR or p120E4F. The possible functional relevance of the interaction between HBx and E4F proteins is discussed in the contexts of cellular transformation and host-virus co-evolution.

Adenovirus E4 Proteins↗

PubMed2004

Lethal mutagens: broad-spectrum antivirals with limited potential for development of resistance?

RNA virus populations display extreme sequence variation. It is thought that this heterogeneity is advantageous to the population, permitting adaptation to rapidly changing environments that present varying types and degrees of selective pressure. A consequence of this efficient evolution of RNA viruses is the susceptibility of these viruses to compounds that further increase sequence variation as these agents force the virus into error catastrophe. Therefore, lethal mutagenesis, induction of error catastrophe, represents an important, untapped strategy for development of antiviral agents. This article briefly describes the theoretical and experimental data supporting lethal mutagenesis as an antiviral strategy and discusses host and viral mechanisms for development of resistance to ribavirin, a representative of this class of antiviral agents.

Antiviral Agents↗

PubMed2001

Timing of the HIV-1 subtype C epidemic in Ethiopia based on early virus strains and subsequent virus diversification.

OBJECTIVE: To trace the introduction of HIV-1 subtype C into Ethiopia based on virus diversification during the epidemic. DESIGN: A set of 474 serum samples obtained in Ethiopia in 1982-1985 was tested for HIV-1. HIV-1 env gp120 V3 and gag or pol regions were sequenced and analysed together with sequences from later stages of the epidemic. RESULTS: None of 98 samples from 1982-1983, one of 193 samples from 1984, and one of 183 samples from 1985 were HIV-1 positive. Phylogenetic analysis of virus sequences from positive samples revealed that they belong to the Ethiopian C, and not the C', cluster. Analysis of 81 Ethiopian C V3 sequences from 1984-1997 revealed that the consensus sequence of the Ethiopian epidemic has been stable over time. Both the 1984 and 1985 V3 sequences, in contrast with three out of 27 (11%) of the 1988 and none out of 51 of the 1992-1997 sequences, had no synonymous substitutions compared to the reconstructed common ancestor of the Ethiopian C viruses. A highly significant correlation between sampling years of the V3 sequences and their synonymous distances to the common ancestor was demonstrated. CONCLUSIONS: The increasing genetic heterogeneity together with stable consensus sequence of the Ethiopian HIV-1 C population demonstrates that evolution of the virus population is characterized by an unbiased expansion around a stationary consensus. Based on the rate of synonymous diversification of HIV-1 strains within the Ethiopian population, we were able to estimate 1983 (95% confidence interval, 1980-1984) as the year of HIV-1 C introduction into Ethiopia.

Adult↗

PubMed2006

Molecular epidemiology and evolution in an outbreak of fulminant hepatitis B virus.

In order to establish the transmission pathway for two outbreak patients affected by fulminant hepatitis B (FHB) following a shared period of hospitalization, we sequenced the complete genomes of the hepatitis B viruses (HBV) isolated from them as well as from the suspected common source and 11 additional controls. Phylogenetic and statistical analyses of these sequences revealed that the two FHB patients were indeed infected by a common source and that the fatal development of the disease did not appear to be associated with any mutation previously reported to be related to FHB. These data have also allowed us to estimate the extent and distribution of genetic variability along the genomes of HBV genotype D samples from the same source population. As a result of these analyses, we provide an improved statistical method to individualize the assignment of each suspected patient and the source of an outbreak and information on which genome region to analyze in the molecular epidemiological assessment of hepatitis B virus transmission cases.

DNA, Viral↗

PubMed2006

High throughput sequencing and comparative genomics of foot-and-mouth disease virus.

Despite a basic understanding of many aspects of FMD biology, much information regarding FMDV virulence, host range, and virus transmission remains poorly understood. Here we present how the use of high throughput sequencing for complete genome sequences of foot-and mouth disease virus (FMDV) led to a series of new insights into viral genome sequence conservation and variability, genetic diversity in nature and phylogenetic classification of isolates, including the first complete sequences of the South African Territories type 1 and 3 (SAT1 and SAT3) genomes. Comparative genomic analysis of full-length sequences of FMDV isolates did allow: (i) the identification of highly conserved regulatory or coding regions which are critical for aspects of virus biology as well as novel viral genomic motifs with likely biological relevance; (ii) characterization of the first complete sequences of the SAT1 and SAT3 genomes; (iii) identification of a novel SAT virus lineage genetically distinct from other SAT and Euro-Asiatic lineages; (iv) precise identification of strains circulating around the world for epidemiological and forensic attribution; (v) assessment of mutation and recombination processes as mechanisms equally involved in evolution; (vi) mutation rates, tolerance and constraints of genes and proteins during evolution of FMD viruses during in vivo replication and (vi) support for the hypothesis of a new evolutionary model.

Animals↗

PubMed1993

Evolution of sequence divergence among human immunodeficiency virus type 1 isolates derived from a blood donor and a recipient.

Four neonates who were infected with a single unit of blood from a human immunodeficiency virus-1 (HIV-1)-infected adult (patient 1) were studied. Two of the infected children (patients II and III) developed symptomatic HIV-1 disease and died within the first 3 y of life. One child (patient IV) died at 8 mo of age of clinical problems that may have been HIV-related. In contrast, one child (patient V) has remained asymptomatic for 7.5 y and has exhibited a very gradual decline in CD4+ cell number. A previous study had shown very limited sequence diversity of isolates from patients I, II, and III (McNearney T et al.: Proc Natl Acad Sci USA 87:1917-1921, 1990). The current study examined additional HIV-1 sequences encoding the principal neutralizing V3 loop of the surface envelope protein of isolates from patients I and V. Amplified sequences were obtained using the polymerase chain reaction from a cultured isolate and uncultured peripheral blood leukocytes, and nucleotide sequences were determined for 13 clones from patient I and 19 clones from patient V. Clones derived from the cultured isolate exhibited less predicted amino acid sequence diversity on average (0-5.2%) than did sequences from uncultured leukocytes (0-19.8% differences). All clones were more closely related to those from patients II and III (0-19.8% amino acid differences) than to other North American or European isolates (18.8-27.0% amino acid differences) or African isolates (41.0-48.0% amino acid differences). Substitutions occurred at sites predicted to modulate host cell tropism and proteolytic cleavage of the V3 loop.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗