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PubMed2002

Dominance of CD8 responses specific for epitopes bound by a single major histocompatibility complex class I molecule during the acute phase of viral infection.

Cytotoxic T-lymphocyte (CTL) responses are thought to control human immunodeficiency virus replication during the acute phase of infection. Understanding the CD8(+) T-cell immune responses early after infection may, therefore, be important to vaccine design. Analyzing these responses in humans is difficult since few patients are diagnosed during early infection. Additionally, patients are infected by a variety of viral subtypes, making it hard to design reagents to measure their acute-phase immune responses. Given the complexities in evaluating acute-phase CD8(+) responses in humans, we analyzed these important immune responses in rhesus macaques expressing a common rhesus macaque major histocompatibility complex class I molecule (Mamu-A*01) for which we had developed a variety of immunological assays. We infected eight Mamu-A*01-positive macaques and five Mamu-A*01-negative macaques with the molecularly cloned virus SIV(mac)239 and determined all of the simian immunodeficiency virus-specific CD8(+) T-cell responses against overlapping peptides spanning the entire virus. We also monitored the evolution of particular CD8(+) T-cell responses by tetramer staining of peripheral lymphocytes as well as lymph node cells in situ. In this first analysis of the entire CD8(+) immune response to autologous virus we show that between 2 and 12 responses are detected during the acute phase in each animal. CTL against the early proteins (Tat, Rev, and Nef) and against regulatory proteins Vif and Vpr dominated the acute phase. Interestingly, CD8(+) responses against Mamu-A*01-restricted epitopes Tat(28-35)SL8 and Gag(181-189)CM9 were immunodominant in the acute phase. After the acute phase, however, this pattern of reactivity changed, and the Mamu-A*01-restricted response against the Gag(181-189)CM9 epitope became dominant. In most of the Mamu-A*01-positive macaques tested, CTL responses against epitopes bound by Mamu-A*01 dominated the CD8(+) cellular immune response.

Acute Disease↗
PubMed1996

Can evolutionary principles help resolve the acquired immune deficiency syndrome crisis?

The population of retroviruses inside each infected host can quickly adapt its genes in response to survival threats. For this reason, therapeutics attempting to eliminate or inhibit the human immunodeficiency virus have been unsuccessful. However, it may be possible to apply evolutionary principles to the problem of human immunodeficiency virus infection/acquired immune deficiency syndrome. The rapid evolution capabilities of this pathogen might assist researchers in evolving human immunodeficiency virus toward the goal of virus-host coexistence. In this relationship, infecting viruses do not harm their host. Two different examples illustrate the theoretical application of evolutionary principles to this problem. First, by viewing the virus as a new gene of the immune system, it is possible to evolve this gene toward the goal of improving immune function. Second, the retroviral population of each host is maladapted for long-term survival. Retroviral genes could be evolved with respect to continued existence in the host.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Evaluation of a new hepatitis C virus sequencing assay as a routine method for genotyping.

The determination of HCV genotypes, subtypes and isolates has been helpful in understanding the evolution and the epidemiology of the virus, and is an important factor in the pre-treatment evaluation. A new simpler and automated sequencing based system has been developed recently, the Visible Genetics TruGene Hepatitis C Assay. The aim of the study was to compare this new genotyping assay with reverse hybridization based Innogenetics INNO-LiPA HCV II assay that is used most commonly. Eighty-eight HCV-RNA positive patients were enrolled and divided in four groups: 26 hemodialysed patients, 30 untreated patients with chronic HCV hepatitis, 12 IFN non-responder patients with chronic HCV hepatitis, 20 asymptomatic HCV positive subjects. The 5'-UTR region was amplified by RT-PCR and the nucleotide sequences determined by the TruGene assay. In parallel, the amplicons were also tested by INNO-LiPA. Concordant results were obtained in 80 out of 88 cases (90.9%). The new assay allowed to genotype 2 samples not typed by LiPA as 1b and 2a/c. The new system also allowed the subtyping of 3 untypable samples, classified as genotype 1 by INNO-LiPA, as genotype 1b (1 sample) and, as genotype 4 (2 samples). The difference between these genotype 4 isolates and the closest genotype 1 isolate was 6 nucleotides. One LiPA genotype 1a sample was typed as 1b and 2 genotype 1b samples were all typed as 1a by the sequence analysis. In conclusion, the new assay is a sensitive and rapid method that is suitable for accurate large-scale genotyping.

5' Untranslated Regions↗
PubMed2006

Feline lentivirus evolution in cross-species infection reveals extensive G-to-A mutation and selection on key residues in the viral polymerase.

Factors that restrict a virus from establishing productive infection in a new host species are important to understand because cross-species transmission events are often associated with emergent viral diseases. To determine the evolutionary pressures on viruses in new host species, we evaluated the molecular evolution of a feline immunodeficiency virus derived from a wild cougar, Puma concolor, during infection of domestic cats. Analyses were based on the coding portion of genome sequences recovered at intervals over 37 weeks of infection of six cats inoculated by either intravenous or oral-nasal routes. All cats inoculated intravenously, but only one inoculated orally-nasally, became persistently viremic. There were notable accumulations of lethal errors and predominance of G-to-A alterations throughout the genome, which were marked in the viral polymerase gene, pol. Viral structural (env and gag) and accessory (vif and orfA) genes evolved neutrally or were under purifying selection. However, sites under positive selection were identified in reverse transcriptase that involved residues in the nucleotide binding pocket or those contacting the RNA-DNA duplex. The findings of extensive G-to-A alterations in this cross-species infection are consistent with the recently described editing of host cytidine deaminase on lentivirus genomes. Additionally, we demonstrate that the primary site of hypermutation is the viral pol gene and the dominant selective force acting on this feline immunodeficiency virus as it replicates in a new host species is on key residues of the virus polymerase.

Animals↗
PubMed1986

Relationship between mitogenic activity of influenza viruses and the receptor-binding specificity of their hemagglutinin molecules.

The relationship between the mitogenic activity of influenza type A viruses for murine B lymphocytes and the receptor-binding specificity of their hemagglutinin was examined. Receptor-binding specificity was determined by the ability of the virus to agglutinate erythrocytes that had been sialidase treated and then enzymatically resialylated to contain sialyloligosaccharides with defined sequences. Distinct differences in receptor-binding specificity were observed between strongly and weakly mitogenic viruses of the H3 subtype, with strong mitogenic activity correlating with the ability of the virus to recognize the sequence N-glycolylneuraminic acid alpha 2,6 galactose (NeuGc alpha 2,6Gal). Viruses isolated early in the evolution of the H3 subtype (from 1968 to 1971) are relatively weak mitogens and recognize the sequence N-acetylneuraminic acid alpha 2,6 galactose (NeuAc alpha 2,6Gal) but not NeuGc alpha 2,6Gal. H3 viruses isolated since 1972 are strongly mitogenic, and these viruses recognize both NeuGc alpha 2,6Gal and NeuAc alpha 2,6Gal. The amino acid substitution of Tyr for Thr at residue 155 of HA1 may be critical to this change in receptor-binding specificity and mitogenic activity of the later H3 viruses. Horse serum-resistant variants of H3 viruses, which bind preferentially to the sequence NeuAc alpha 2,3Gal, are poorly mitogenic. Differences were also observed between the receptor-binding specificity of the strongly mitogenic H3 viruses and viruses of the H2 and H6 subtypes, the mitogenic activity of which is limited to strains of mice that express the class II major histocompatibility complex glycoprotein I-E. The results indicate that the receptor-binding specificity of the hemagglutinin plays a critical role in determining the mitogenic activity of influenza viruses.

B-Lymphocytes↗
PubMed1979

[Use of serum s-IgA detection in liver pathology (author's transl)].

Secretory IgA (sIgA) were searched in 60 sera of healthy blood donors and in 1 590 sera of subjects having various diseases. 20 percent of these subjects showed an increased amount of sIgA in their sera. The only subjects presenting a constant increase (sometimes more than 20 fold the normal amount) were people with liver diseases. Quantitation of sIgA, in relation with the determination of the IgA/transferrin ratio (IgA/T) in sera, showed an important difference between Laennec's cirrhosis on one hand and virus hepatitis or post-hepatitic cirrhosis on the other. In Laennec's cirrhosis a moderate increase in sIgA went with a strong elevation of the IgA/T ratio, the latter being proportional to the degree of evolution of the disease. In virus hepatitis, the sIgA amount was largely increased while the IgA/T ratio remained at a normal value.

Hepatitis, Viral, Human↗
PubMed1994

A primate T-lymphotropic virus, PTLV-L, different from human T-lymphotropic viruses types I and II, in a wild-caught baboon (Papio hamadryas).

Searching for clues to the evolution of the primate T-lymphotropic viruses (PTLVs), which include the human and the simian T-lymphotropic viruses (HTLV and STLV), we have identified another PTLV, which differs sufficiently from the known PTLV-I and PTLV-II types to be designated here PTLV-L. The virus was isolated from a wild-born baboon (Papio hamadryas) from Eritrea. In a cDNA library a 1802-bp-long fragment was identified that extends from the env region, including the complete transmembrane protein gene, to part of the tax/rex gene. Homologies at the nucleotide sequence level of PTLV-L, prototype simian T-lymphotropic virus-PH969, with HTLV-I and -II, respectively, were 62% and 64% overall, 65% and 70% in the env region, and 80% and 80% in the partial tax/rex sequence. In the 5' part of the pX region a significant homology was seen only with HTLV-II (52%). Phylogenetic analysis based on the gene encoding the transmembrane protein indicates that PTLV-L represents a PTLV type with a long independent evolution, longer than any strain within the PTLV-I or PTLV-II groups. The finding of another PTLV type in African baboons is further evidence of the wide variety of PTLV found on this continent. Whether PTLV-L resembles PTLV-I and PTLV-II in the extension of its host range to other primates, including humans, remains to be seen.

Amino Acid Sequence↗
PubMed1987

Evolution of in vitro persistence of two strains of canine parainfluenza virus. Brief report.

Lytic stock virus (CPI+) exhibited prominent CPE in Vero cell monolayers. The non-syncytial giant cell forming strain (CPI-) was isolated from brain tissues of a dog after experimental infection with syncytial giant cell-forming (CPI+) virus. In mixed infection experiments, CPI(-) virus interfered with the replication of CPI(+) virus in that simultaneously infected cells showed strand-forming CPE typical of CPI(-) and reduction of CPI(+) yield. The CPI(-) virus established immediate in vitro persistence, followed by a severe crisis at passage (p) 8 and several similar crises until p 31; no further crises occurred throughout the remaining observation period (p 80). The CPI(+) did not establish immediate in vitro viral persistence and experienced several lytic crises until p 29. No further crises were observed throughout the observation period (p 100).

Animals↗
PubMed2005

Evolution of the intrahepatic T cell repertoire during chronic hepatitis C virus infection.

Chronic hepatitis C virus (HCV) infection is characterized by extensive infiltration of inflammatory cells in the liver, where there is a compartmentalization of HCV-reactive T lymphocytes. Previous studies have demonstrated a broad intrahepatic TCR repertoire; however, there is little information regarding the stability of this intrahepatic T cell population. We studied the T cell repertoires in sequential liver biopsy samples from five individuals with chronic HCV infection using TCR spectratype analysis; four subjects had been treated with IFN-alpha during the interval between biopsies. Transcripts from most TCRBV families were detectable in the liver tissues, and 25-85% of these had skewed spectratype profiles indicative of T cell clonal expansions. Most of the intrahepatic T cell expansions were not evident in an analysis of peripheral blood T cells collected at the same time as the liver biopsy. Detailed analysis using TCRBJ-primed run-off reactions revealed that the intrahepatic TCR repertoires were not stable within an individual, although some TCR clonotypes were maintained for at least 45 months.

Biopsy↗
PubMed1998

Evolution of syncytium-inducing and non-syncytium-inducing biological virus clones in relation to replication kinetics during the course of human immunodeficiency virus type 1 infection.

To investigate the temporal relationship between human immunodeficiency virus type 1 (HIV-1) replicative capacity and syncytium-inducing (SI) phenotype, biological and genetic characteristics of longitudinally obtained virus clones from two HIV-1-infected individuals who developed SI variants were studied. In one individual, the emergence of rapidly replicating SI and non-syncytium-inducing (NSI) variants was accompanied by a loss of the slowly replicating NSI variants. In the other subject, NSI variants were always slowly replicating, while the coexisting SI variants showed an increase in the rate of replication. Irrespective their replicative capacity, the NSI variants remained present throughout the infection in both individuals. Phylogenetic analysis of the V3 region showed early branching of the SI variants from the NSI tree. Successful SI conversion seemed a unique event since no SI variants were found among later-stage NSI variants. This was also confirmed by the increasing evolutionary distance between the two subpopulations. At any time point during the course of the infection, the variation within the coexisting SI and NSI populations did not exceed 2%, indicating continuous competition within each viral subpopulation.

Amino Acid Sequence↗
PubMed2000

Evolution of nutritional status of infants infected with the human immunodeficiency virus.

CONTEXT: There are today only a limited number of studies defining growth parameters and nutritional status for HIV children. OBJECTIVE: To study the nutritional status of infants infected with the human immunodeficiency virus. TYPE OF STUDY: Longitudinal study. SETTING: Department of Pediatrics, Faculty of Medical Sciences, UNICAMP, Campinas, Brazil. PARTICIPANTS: One hundred and twenty-four children born to HIV infected mothers were evaluated from birth until the age of two years. They were subdivided into two groups: 71 infected children and 53 non-infected children. MAIN MEASUREMENTS: Growth was evaluated in both groups by comparing Z-scores for weight/age (w/a), length/age (H/a) and weight/length (w/H) (using the NCHS curves as reference). RESULTS: The Z-score analyses showed that there was a significant difference between the two groups for all the variables studied, except for the H/a value at 3 months of age and the W/H value at 21 months of age, which showed P > 0.05. CONCLUSIONS: The growth of infected infants was observed to be severely affected in comparison with that of seroreversed infants in the same age groups. Although clinical manifestations may take time to appear, the onset of growth changes begin soon after birth.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Clonal selection, clonal senescence, and clonal succession: the evolution of the T cell response to infection with a persistent virus.

We have analyzed the CD8(+) T cell response to EBV and find that a larger primary burst size is associated with proportionally greater decay during the development of memory. Consequently, immunodominance and clonal dominance are less marked in memory than primary responses. An intuitive interpretation of this finding is that there is a limit to the number of cell divisions a T cell clone can undergo, and that the progeny of clones that have expanded massively during a primary immune response are more prone to die as a result of senescence. To test this hypothesis, we have derived a mathematical model of the response of different T cell clones of varying avidity for Ag in the primary and persistent phases of viral infection. When cellular survival and replication are linked to T cell avidity for Ag and Ag dose, then high-avidity T cells dominate both the primary and secondary responses. We then incorporated a limit in the number of cell divisions of individual T cell clones to test whether such a constraint could reproduce the observed association between cell division number and alterations in the contribution of clones to the response to persistent infection. Comparison of the model output with the experimental results obtained from primary and persistent EBV infection suggests that there is indeed a role for cellular senescence in shaping the immune response to persistent infection.

Cell Differentiation↗
PubMedDate not supplied

[The evolution of pulmonary tuberculosis in health area no 4 in Valencia during the period 1988-1993].

BACKGROUND: Morbidity from Pulmonary tuberculosis, detected by the system EDO in the Autonomous Community of Valencia, shows an increasing trend and differential behaviour in relation with age and constitutes, with no doubt, a Public Health problem involving a joint action of multiple clinical care and preventive units. METHODS: In our study, the cases of notified and confirmed pulmonary tuberculosis over the period 1988-1993 in the Health Area number 4 (Region Camp de Morvedre 167.744 inhabitants) are analyzed by estimating the evolution of incidence, the diagnosis time and place where this diagnosis was made in accordance with the conventional variables of ecological studies and excluding from our registry the cases of those patients with co-infection by virus VIH. RESULTS: The growing evolution of incidence, the mean rate for the period (49.95.10(5) h.), the rate differential per age-groups during the period and the concentration of cases in the young age-groups (15-39 years) constitute, together with the diagnosis time (75.6 days in Primary Health Care; 74.3 in Hospital), the most outstanding results. Nevertheless, the prolongation of the diagnosis time for order age-groups (140-168 days in people older than 54 years) and the absence of a previous known contact, suggest the presence of undetected cases of TBC and dissemination ways other than the interfamily ones. CONCLUSIONS: An improved notification and identification of cases from hospital sources involves the necessity of reducing the mean diagnosis time and the research on the ways of transmission other than the interfamily ones; this explains a limited part of the incidence.

Adolescent↗
PubMed2002

Factors related to the chronicity and evolution of hepatitis C infection in patients co-infected by the human immunodeficiency virus.

OBJECTIVES: This work analyses the influence of immune status, serum human immunodeficiency virus (HIV) load and hepatitis C virus (HCV) genotypes on the probability of resolution of HCV infection in HIV-co-infected patients, as well as the evolution of HCV viremia after antiretroviral therapy. PATIENTS AND METHODS: Forty-five patients with anti-HIV and anti-HCV antibodies were classified into two groups as a function of the positivity or persistent negativity of HCV RNA detection (active or recovered HCV infection, respectively). They were treated with highly active antiretroviral therapy (HAART). Serum HCV RNA was quantified by the reverse transcription-polymerase chain reaction. HCV genotypes were detected by line probe assay or by detection of type-specific antibodies. RESULTS: HCV RNA was detectable in 30 (66.6%) out of 45 HIV-infected patients. CD4+ T-cell counts, HIV viremia, or HCV genotypes were similar in patients with active or recovered HCV infection. Patients with active HCV infection had a non-significant decrease of HCV viremia during a follow-up of 12 months (from 6.15 +/- 6.32 to 5.96 +/- 6.05 log copies/mL). This was not influenced by baseline HCV or HIV viral load, HCV genotype, or CD4+ T-cell count. The non-significant decrease was present in patients with or without an immunological response to HAART. CONCLUSION: HCV genotypes, immune status, or serum HIV load did not influence the resolution or chronicity of HCV infection in HIV-co-infected individuals. A non-significant decrease of HCV viremia in these patients treated with combinations including antiproteases could be expected.

Adult↗