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PubMed2001

Efficacy of vaccination of pigs with different H1N1 swine influenza viruses using a recent challenge strain and different parameters of protection.

This study investigates whether antigenic evolution within H1N1 swine influenza viruses can compromise vaccine efficacy and, specifically, whether the A/New Jersey/8/76 strain in the commercial swine influenza vaccines needs to be updated. Pigs were vaccinated twice intramuscularly with experimental monovalent vaccines derived from different H1N1 strains (A/New Jersey/8/76, Sw/Belgium/1/83 or Sw/Belgium/1/98) or with a commercial bivalent vaccine based on A/New Jersey/8/76 (H1N1) and A/Port Chalmers/1/73 (H3N2). Experimental and commercial vaccines contained a different adjuvant. Two weeks after the second vaccination, all pigs were challenged intratracheally with Sw/Belgium/1/98. Mean pre-challenge haemagglutination inhibition (HI) antibody titres against the challenge virus were lower for the experimental A/New Jersey/8/76 vaccine than for the other vaccines. The reduction in mean virus titres in the lungs was highly significant for the latter vaccines, including the commercial New Jersey-derived vaccine, but not for the experimental A/New Jersey/8/76 vaccine. Clinical signs after challenge were negligible in all vaccinates. Post-challenge levels of interferon-alpha and tumor necrosis factor-alpha in bronchoalveolar lavage fluids were reduced in the vaccinates, while levels of interleukin-1 and neutrophils were less consistent. Though the A/New Jersey/8/76 strain is less effective in preventing infection by Sw/Belgium/1/98 than the homologous virus or than Sw/Belgium/1/83, all strains can protect completely if antibody titres against the challenge virus are sufficiently high. Apart from the vaccine strain, adjuvant and antigenic dose may play a crucial role in vaccine efficacy.

Animals↗
PubMed2004

Exonic splicing enhancers in fission yeast: functional conservation demonstrates an early evolutionary origin.

Discrete sequence elements known as exonic splicing enhancers (ESEs) have been shown to influence both the efficiency of splicing and the profile of mature mRNAs in multicellular eukaryotes. While the existence of ESEs has not been demonstrated previously in unicellular eukaryotes, the factors known to recognize these elements and mediate their communication with the core splicing machinery are conserved and essential in the fission yeast Schizosaccharomyces pombe. Here, we provide evidence that ESE function is conserved through evolution by demonstrating that three exonic splicing enhancers derived from vertebrates (chicken ASLV, mouse IgM, and human cTNT) promote splicing of two distinct S. pombe pre-messenger RNAs (pre-mRNAs). Second, as in extracts from mammalian cells, ESE function in S. pombe is compromised by mutations and increased distance from the 3'-splice site. Third, three-hybrid analyses indicate that the essential SR (serine/arginine-rich) protein Srp2p, but not the dispensable Srp1p, binds specifically to both native and heterologous purine-rich elements; thus, Srp2p is the likely mediator of ESE function in fission yeast. Finally, we have identified five natural purine-rich elements from S. pombe that promote splicing of our reporter pre-mRNAs. Taken together, these results provide strong evidence that the genesis of ESE-mediated splicing occurred early in eukaryotic evolution.

Animals↗
PubMed2002

Immune responses to myxoma virus.

Myxoma virus causes the systemic disease myxomatosis in the European rabbit (Oryctolagus cuniculus). Originating in the South American rabbit Sylvilagus brasiliensis, where it causes a relatively localized fibroma, myxoma virus is a classic example of a virus that has jumped species to produce an exotic disease and then coevolved with its new host. Like other poxviruses, myxoma virus encodes multiple proteins capable of downregulating the host innate and acquired immune responses. Other virus-encoded proteins enable replication in host lymphocytes and monocytes, for example, by inhibiting apoptosis. Detailed studies on these proteins have demonstrated novel methods of interactions with the host immune system and added substantially to the understanding of the interaction of large DNA viruses with their hosts. Despite the increasingly detailed molecular knowledge of myxoma virus, relatively little is known about the dynamics of the interaction of the virus with the integrated host-immune system during infection and, in particular, about the evolution of resistance to the virus in wild rabbits or the species barrier. This review will focus on the detailed molecular studies that have been done with myxoma virus and discuss the more limited knowledge of the pathogenesis of myxoma virus in rabbits and the ways that the consolidated immune responses may determine genetic resistance to myxomatosis.

Animals↗
PubMed2006

Evolution of complexity in the viral world: the dawn of a new vision.

Recent sequencing of the genomes of numerous large viruses provide for unprecedented opportunities to study the emergence and evolution of complexity in the virus world. This special issue of Virus Research explores trends in the evolution of complex genomes in most major classes of viruses.

Evolution, Molecular↗
PubMed2001

[Serum levels of soluble CD30 molecule in hepatitis B virus infection].

BACKGROUND: The release of CD30 molecule in the soluble form (sCD30) is considered a feature of Th2 activation and proliferation of the cellular phenotype Th2. AIM: To analyze the immunoregulatory role of sCD30 in the evolution of hepatitis B virus (HBV) infection. PATIENTS AND METHODS: Three study groups were formed: 15 patients with acute infection by HBV who remitted toward the resolution of the infection; 15 patients who evolved to the carrier state and 15 subjects without clinical history of infection by this or other viruses. The determination of serological markers for the HBV was done by the Microparticles Enzymatic Immunoanalysis techniques (MEIA). The method of double antibody by ELISA was used For sCD30 determination. RESULTS: A significant sCD30 increase (p < 0.05) was observed in patients with acute infection, during the acute phase (135.7 +/- 36.7). These values decreased to 16.2 +/- 2.5 during the convalescent phase. Patients that evolved to the carrier state, did not experience a rise in sCD30 values (40.2 +/- 6.7, 38 +/- 9.2 and 36.1 +/- 8.3 during the acute phase, at 120 and 240 days respectively). The value in the control group was 34.8 +/- 6.7. CONCLUSIONS: The group that evolved towards remission experienced a higher activation of the Th2 cellular phenotype, promoting humoral immune response. An inactivity of sCD30 values was observed in the group that evolved to the carrier state.

Adolescent↗
PubMed1995

Phylogenetic analysis of Leishmania RNA virus and Leishmania suggests ancient virus-parasite association.

Some strains of the protozoan parasite Leishmania belonging to the new world species guyanensis and braziliensis are infected with persistent, single-segmented, non-enveloped dsRNA viruses termed LRV1. A single old world strain classified as L. major was recently found to harbor a similar virus, designated LRV2-1. The genomic nucleotide sequences of two LRV1 types (1-1 and 1-4) isolated from two L. guyanensis strains have been determined and found to be highly conserved. In contrast, LRV1-specific cDNA probes derived from the conserved genomic 5' region failed to recognize LRV2 RNA on Northern blots, suggesting a greater degree of divergence between LRV1 and LRV2 than among LRV1 types. This observation suggests a long-term association and coevolution of LRV within each parasite strain. We tested this concept by comparing nucleotide sequences of seven LRV types and PCR fingerprints of the parasite strains from which these viruses were derived. In support of the idea of virus-parasite co-evolution, we find that genetic distances between LRV types mirror the heterogeneity between parasite fingerprints and are clustered according to the geographical origin of the strains. In agreement with the postulated common origin of persistent dsRNA viruses of protozoa and fungi, we conclude that the infection of Leishmania with LRV pre-dates the divergence of Leishmania into different lineages.

Amino Acid Sequence↗
PubMed1997

Recombinational history and molecular evolution of western equine encephalomyelitis complex alphaviruses.

Western equine encephalomyelitis (WEE) virus (Togaviridae: Alphavirus) was shown previously to have arisen by recombination between eastern equine encephalomyelitis (EEE)- and Sindbis-like viruses (C. S. Hahn, S. Lustig, E. G. Strauss, and J. H. Strauss, Proc. Natl. Acad. Sci. USA 85:5997-6001, 1988). We have now examined the recombinational history and evolution of all viruses belonging to the WEE antigenic complex, including the Buggy Creek, Fort Morgan, Highlands J, Sindbis, Babanki, Ockelbo, Kyzylagach, Whataroa, and Aura viruses, using nucleotide sequences derived from representative strains. Two regions of the genome were examined: sequences of 477 nucleotides from the C terminus of the E1 envelope glycoprotein gene which in WEE virus was derived from the Sindbis-like virus parent, and 517 nucleotide sequences at the C terminus of the nsP4 gene which in WEE virus was derived from the EEE-like virus parent. Trees based on the E1 region indicated that all members of the WEE virus complex comprise a monophyletic group. Most closely related to WEE viruses are other New World members of the complex: the Highlands J, Buggy Creek, and Fort Morgan viruses. More distantly related WEE complex viruses included the Old World Sindbis, Babanki, Ockelbo, Kyzylagach, and Whataroa viruses, as well as the New World Aura virus. Detailed analyses of 38 strains of WEE virus revealed at least 4 major lineages; two were represented by isolates from Argentina, one was from Brazil, and a fourth contained isolates from many locations in South and North America as well as Cuba. Trees based on the nsP4 gene indicated that all New World WEE complex viruses except Aura virus are recombinants derived from EEE- and Sindbis-like virus ancestors. In contrast, the Old World members of the WEE complex, as well as Aura virus, did not appear to have recombinant genomes. Using an evolutionary rate estimate (2.8 x 10(-4) substitutions per nucleotide per year) obtained from E1-3' sequences of WEE viruses, we estimated that the recombination event occurred in the New World 1,300 to 1,900 years ago. This suggests that the alphaviruses originated in the New World a few thousand years ago.

Alphavirus↗
PubMed1995

Molecular epizootiology and evolution of the glycoprotein and non-virion protein genes of infectious hematopoietic necrosis virus, a fish rhabdovirus.

Infectious hematopoietic necrosis virus (IHNV) causes a highly lethal, economically important disease of salmon and trout. The virus is enzootic throughout western North America, and has been spread to Asia and Europe. The nucleotide sequences of the glycoprotein (G) and non-virion (NV) genes of 12 diverse IHNV isolates were determined in order to examine the molecular epizootiology of IHN, the primary structure and conservation of NV, and the evolution of the virus. The G and NV genes and their encoded proteins were highly conserved, with a maximum pairwise nucleotide divergence of 3.6 and 4.4%, and amino acid divergence of 3.7 and 6.2%, respectively. Conservation of NV protein sequence (111 amino acids in length) confirms that the protein is functional and plays an important role in virus replication. The phylogenetic relationship of viruses was found to correlate with the geographic origin of virus isolates rather than with host species or time of isolation. These data are consistent with stable maintenance of virus in enzootic foci. Two main IHNV genetic lineages were identified; one in the Columbia River Basin (Oregon, Washington and Idaho), the other in the Sacramento River Basin (California). The first major IHNV outbreak in chinook salmon in 1973 in the Columbia River was genetically linked to importation of virus-infected fish eggs from the Sacramento River where outbreaks in chinook salmon are common. However, the introduced virus apparently did not persist, subsequent virus outbreaks in Columbia River chinook salmon being associated with Columbia River genetic lineages. In general, virus monoclonal antibody reactivity profiles and phylogenetic relationships correlated well.

Amino Acid Sequence↗
PubMed1993

Divergence and evolution of homologous regions of Bombyx mori nuclear polyhedrosis virus.

Homologous regions (hrs) (hr1,hr2-left,hr2-right,hr3,hr4-left,hr 4-right, and hr5) similar to those found in the Autographa californica nuclear polyhedrosis virus (AcNPV) genome were found in the Bombyx mori NPV (BmNPV) genome. The BmNPV hrs contained two to eight repeats of a homologous nucleotide sequence which were on average about 75 bp long. All of these homologous sequence repeats contained a 26-bp-long palindrome motif with an EcoRI or EcoRI-like site at its core. The consensus sequence of the BmNPV hrs showed 95% conservation with respect to those found in AcNPV. Nucleotide sequence analysis indicated that hr2-left and hr2-right of BmNPV evolved from an ancestor similar to hr2 of AcNPV by inversion, cleavage, and ligation. The polarities of the BmNPV and AcNPV hrs were conserved except for that of hr4-left. Within hr4-right of BmNPV, four repeats of a previously underscribed palindrome motif were found. Bmhr5D, a BmNPV mutant which lacked hr5, replicated at a rate similar to that of wild-type BmNPV in BmN cells and silkworm larvae, indicating that hr5 was not essential for viral replication. After ten passages of Bmhr5D in BmN cells, no detectable changes in its genome were observed by restriction endonuclease analysis. The evolution and divergence of the BmNPV genome are also discussed.

Animals↗
PubMed1993

Split decomposition: a technique to analyze viral evolution.

A clustering technique allowing a restricted amount of overlapping and based on an abstract theory of coherent decompositions of finite metrics is used to analyze the evolution of foot-and-mouth disease viruses. The emerging picture is compatible with the existence of viral populations with a quasispecies structure and illustrates various forms of evolution of this virus family. In addition, it allows the correlation of these forms with geographic occurrence.

Animals↗
PubMed1994

Genotyping of human T cell lymphotropic virus type I using Australo-Melanesian topotype-specific oligonucleotide primer-based polymerase chain reaction: insights into viral evolution and dissemination.

Sequence variants of human T cell lymphotropic virus type I (HTLV-I), genetically distinct from cosmopolitan strains of HTLV-I from Japan, the Americas, the Caribbean, and Africa, have been discovered among Melanesians in Papua New Guinea and the Solomon Islands and among Australian aboriginals. By using oligonucleotide primer pairs derived from sequences unique to the gp46- and gp21-encoding regions of the env gene of the Melanesian HTLV-I variants, HTLV-I strains from widely separated geographic regions could be grouped into either of two major geographic-specific genotypes or topotypes: Australo-Melanesian and cosmopolitan. These primers did not permit amplification of the corresponding env gene regions in strains of simian T cell lymphotropic virus type I from Asia and Africa. Phylogenetic analysis also supported two distinct lineages, consistent with evolution of HTLV-I in Australia and Melanesia independent from that in other parts of the world.

Australia↗
PubMed1996

Evolution of the haemagglutinin-esterase gene of influenza C virus.

The nucleotide sequences of the haemagglutinin-esterase (HE) genes of 18 influenza C virus strains isolated in Japan during the period from 1964 to 1988 (11 published and 7 new sequences) were analysed to examine their evolutionary relationships. The phylogenetic tree constructed by the maximum parsimony method revealed the existence of four discrete lineages (I to IV), one of which (lineage III) may have died out in the late 1970s. Sequential evolution was demonstrated within seven strains of lineage I, which allowed estimation of an evolutionary rate of 0.49 x 10-3 nucleotide substitutions per site per year, a value corresponding to about one-ninth of the rates of human influenza A virus haemagglutinin genes. In the previously proposed immunodominant region on HE protein (positions 178 to 217), there was little or no amino acid sequence divergence among viruses on the same lineage although considerable divergence was seen among those on different lineages, raising the possibility that immune selection may not have played a significant role in the evolution of the glycoprotein, at least not after separation into lineages occurred. It was also found that the HE genes of the seven isolates obtained outside Japan during 1966-1983 could be each assigned to one of lineages I, II and IV, which suggests that influenza C virus is capable of spreading worldwide.

Amino Acid Sequence↗
PubMed1990

Fitness of RNA virus decreased by Muller's ratchet.

Why sex exists remains an unsolved problem in biology. If mutations are on the average deleterious, a high mutation rate can account for the evolution of sex. One form of this mutational hypothesis is Muller's ratchet. If the mutation rate is high, mutation-free individuals become rare and they can be lost by genetic drift in small populations. In asexual populations, as Muller noted, the loss is irreversible and the load of deleterious mutations increases in a ratchet-like manner with the successive loss of the least-mutated individuals. Sex can be advantageous because it increases the fitness of sexual populations by re-creating mutation-free individuals from mutated individuals and stops (or slows) Muller's ratchet. Although Muller's ratchet is an appealing hypothesis, it has been investigated and documented experimentally in only one group of organisms--ciliated protozoa. I initiated a study to examine the role of Muller's ratchet on the evolution of sex in RNA viruses and report here a significant decrease in fitness due to Muller's ratchet in 20 lineages of the RNA bacteriophage phi 6. These results show that deleterious mutations are generated at a sufficiently high rate to advance Muller's ratchet in an RNA virus and that beneficial, backward and compensatory mutations cannot stop the ratchet in the observed range of fitness decrease.

Bacteriophages↗
PubMed1998

Is the major capsid protein of iridoviruses a suitable target for the study of viral evolution?

Iridoviruses are large cytoplasmic DNA viruses that are specific for different insect or vertebrate hosts. The major structural component of the non-enveloped icosahedral virus particles is the major capsid protein (MCP) which appears to be highly conserved among members of the family Iridoviridae, Phycodnaviridae, and African swine fever virus. The amino acid sequences of the known MCPs were used in comparative analyses to elucidate the phylogenic relationships between different cytoplasmic DNA viruses including three insect iridoviruses (Tipula iridescent virus, Simulium iridescent virus, Chilo iridescent virus), seven vertebrate iridoviruses isolated either from fish (lymphocystis disease virus, rainbow trout virus, European catfish virus, doctor fish virus), amphibians (frog virus 3), or reptiles (turtle virus 3, turtle virus 5), one member of the family Phycodnaviridae (Paramecium bursaria Chlorella virus type 1), and African swine fever virus. These analyses revealed that the amino acid sequence of the MCP is a suitable target for the study of viral evolution since it contains highly conserved domains, but is sufficiently diverse to distinguish closely related iridovirus isolates. Furthermore the results suggest that a substantial revision of the taxonomy of iridoviruses based on molecular phylogeny is required.

Amino Acid Sequence↗
PubMed2004

Selection in context: patterns of natural selection in the glycoprotein 120 region of human immunodeficiency virus 1 within infected individuals.

Evolution of the HIV-1 V3 loop was monitored in 15 subjects over a period of 5 years at approximately 6-month intervals. Putative recombination was detected in many of the sequences. Evolutionary trees were estimated from the nonrecombinant viral sequences found in each individual. Selection and altered demographic regimes were detected with logit and other contingency analyses in a highly context-dependent fashion. Mutations leading to amino acid substitutions are subject to positive selection over a broad range of clinical conditions in the nonsyncytium-inducing (NSI) form, and the growth rates of the NSI strains and their level of genetic subdivision change little in going from a healthy immune system to a severely compromised immune system. In contrast, the SI form has a significant increase in growth rate as the immune system goes from healthy to compromised, particularly in those subjects who did not receive any antiviral drug therapy. This increase in SI growth rate results in a significant growth advantage of SI over NSI when the immune system is compromised. The SI strains also show more demographic subdivision when the immune system is healthy than when the immune system is compromised, and the SI form has greater demographic subdivision than NSI in subjects with healthy immune systems who also are not receiving antiviral drug therapy. Positive selection on amino-acid-changing mutations weakens and then intensifies again in the SI strains in going from healthy to compromised immune systems. These patterns are consistent with other studies that suggest that NSI strains inhibit replication of SI strains, that the V3 loop is more hidden from the immune system in the NSI form, that evolution in the V3 loop influences cell tropism and coreceptor usage, that substrate for replication of SI forms increases as the disease progresses, and that death of CD8 cells is influenced by the type of coreceptor usage typically found in SI but not in NSI strains. Finally, the transition between NSI and SI forms is associated with a burst of evolutionary change due to strong positive selection at sites other than those that define the NSI/SI phenotypes.

Acquired Immunodeficiency Syndrome↗
PubMed2004

[Emergence and species barriers].

Emergent viral infections are defined as those the incidence of which has increased over the last 20 years. These infections concern human but also animal viruses affecting wild or tame animals. In humans, emergent viruses are of zoonotic origin and often due to crossing of species barrier. This inter-species crossing is promoted by various circumstances: environmental and climatic variations, bioterrorism, evolutive potential of the virus, etc. Screening for the animal reservoir is extremely important to prevent re-emergence and to eradicate the disease. The emergential success of some viruses has had serious consequences on human public health: flu pandemics, AIDS pandemic, hemorrhagic fever, and more recently SARS.

Animals↗
PubMed2006

Hot crenarchaeal viruses reveal deep evolutionary connections.

The discovery of archaeal viruses provides insights into the fundamental biochemistry and evolution of the Archaea. Recent studies have identified a wide diversity of archaeal viruses within the hot springs of Yellowstone National Park and other high-temperature environments worldwide. These viruses are often morphologically unique and code for genes with little similarity to other known genes in the biosphere, a characteristic that has complicated efforts to trace their evolutionary history. Comparative genomics combined with structural analysis indicate that spindle-shaped virus lineages might be unique to the Archaea, whereas other icosahedral viruses might share a common lineage with viruses of Bacteria and Eukarya. These studies provide insights into the evolutionary history of viruses in all three domains of life.

Archaeal Viruses↗