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PubMed2006

Phycodnaviruses: a peek at genetic diversity.

The family Phycodnaviridae encompasses a diverse collection of large icosahedral, dsDNA viruses infecting algae. These viruses have genomes ranging from 160 to 560kb. The family consists of six genera based initially on host range and supported by sequence comparisons. The family is monophyletic with branches for each genus, but the phycodnaviruses have evolutionary roots that connect with several other families of large DNA viruses, referred to as the nucleocytoplasmic large DNA viruses (NCLDV). The genomes of members in three genera in the Phycodnaviridae have recently been sequenced and the purpose of this manuscript is to summarize these data. The viruses have diverse genome structures, some with large regions of non-coding sequence and others with regions of single-stranded DNA. Typically, phycodnaviruses have the coding capacity for hundreds of genes. The genome analyses have revealed in excess of 1000 unique genes, with only 14 homologous genes held in common among the three genera of the phycodnavirses sequenced to date. Thus, the gene diversity far exceeds the number of so-called "core" genes. Little is known about the replication of these viruses, but the consequences of these infections of the phytoplankton have global affects, including altered geochemical cycling and weather patterns.

DNA Viruses↗
PubMed1999

Molecular characterization of the Japanese encephalitis virus representative immunotype strain JaGAr 01.

We determined the full genomic sequence of the Japanese encephalitis virus JaGAr 01 strain and its predicted amino acid sequence. Nucleotide sequence comparison with ten fully sequenced JE strains shows a homology range from 89.62 to 99.49%. Amino acid sequence homologies range from 96.85 to 99.74%. Comparison of amino acid sequences shows a unique amino acid, arginine, for JaGAr 01 at position 123 of the E-protein, while the eight other strains contained serine. Secondary structure prediction by free energy minimization shows a unique structure for JaGAr 01 that includes an RNA segment that is conserved for all flaviviruses. Speculation is made about the role these results may play in the replication and antigenic characteristics of JaGAr 01. Phylogenetic analyses of the E-protein of JaGAr 01 together with 35 other JE strains showed diversity in amino acid characteristics between the prototype strains Nakayama, JaGAr 01 and Beijing-1. Phylogenetic trees computed by neighbor joining and Fitch Margoliash analysis of nucleic acid and protein sequences showed Nakayama and Beijing in one cluster different from JaGAr 01.

Amino Acid Sequence↗
PubMed1997

[Etiological aspects of reactive hemophagocytoses: retrospective study in 99 patients].

We describe the causes of reactive hemophagocytic process in a retrospective study including 99 patients. The main diagnosis were: lymphomas (18 cases), pyogenic bacteria infections (15 cases), herpes virus infections (12 cases), other infections (multiple, parasitic, fungal, mycobacterial, unidentified) (11 cases), acute hepatitis (five cases), systemic lupus erythematosus (three cases). We also found numerous other diseases involving the reticuloendothelial system. The cause remained undetermined in 16 cases. Lymphoma accounted for 64% of the cases in previously healthy patients who had been febrile for more than 10 days at the time of the diagnosis of reactive hemophagocytic process, and for 31% in HIV-positive patients. Lymphomas were rare (5%) in non HIV-positive, immunosuppressed patients. In this setting and in previously healthy patients who had been febrile for less than 10 days, infectious diseases were widely dominant (respectively 60% and 86% of the cases). Those were mainly due to pyogenic bacteria and to herpes virus. A rapidly fatal evolution occurred in some cases of lymphomas-related hemophagocytic process. These data support the choice of aggressive investigations in order to diagnose lymphoma in previously healthy patients presenting with reactive hemophagocytic process who have been febrile for more than 10 days, and in selected HIV-patients. Such a procedure is not recommended in the other cases.

Adolescent↗
PubMed1999

Nucleotide sequence of a 5892 base pairs fragment of the LsMNPV genome and phylogenetic analysis of LsMNPV.

A 5892 bp fragment of Leucania separata multiple nuclear polyhederosis virus (LsMNPV) containing gp37, 39 k genes and another four ORFs was sequenced in this article. According to regulatory elements on 5' uncoding sequences, the ORF4 and ORF1 are probably two novel baculovirus genes, and the ORF4 probably also is a new early-late gene. The possible functions about GP37 and 39 K proteins were explored. The homology of GP37 protein among LsMNPV and 8 other insect virus was compared. The evolutional position of LsMNPV is also estimated based on the homology of gp37 genes. The structure and its homology of several genes in LsMNPV prove that LsMNPV is far related with other baculovirus and has an exceptional genome organization.

Amino Acid Sequence↗
PubMed2006

Viruses of the Archaea: a unifying view.

DNA viruses of the Archaea have highly diverse and often exceptionally complex morphotypes. Many have been isolated from geothermally heated hot environments, raising intriguing questions about their origins, and contradicting the widespread notion of limited biodiversity in extreme environments. Here, we provide a unifying view on archaeal viruses, and present them as a particular assemblage that is fundamentally different in morphotype and genome from the DNA viruses of the other two domains of life, the Bacteria and Eukarya.

Archaea↗
PubMed1999

Evolution of vaginal Candida species recovered from human immunodeficiency virus-infected women receiving fluconazole prophylaxis: the emergence of Candida glabrata? Terry Beirn Community Programs for Clinical Research in AIDS (CPCRA).

The effect of fluconazole prophylaxis on the vaginal flora of 323 human immunodeficiency virus-infected women was evaluated in a multicenter, randomized, double-blind, placebo-controlled trial. Women with CD4 cell counts of < or = 300/mm3 received either 200 mg of fluconazole per week or placebo. Vaginal surveillance cultures were performed every 3 months. After a follow-up of 29 months, Candida albicans was recovered from 53% of patients receiving fluconazole and 68% of patients assigned placebo. Fluconazole was associated with a 50% reduction in the odds of being colonized with C. albicans but with higher rates for non-albicans Candida species. Candida glabrata was recovered from 40 women assigned fluconazole and 29 assigned placebo (relative odds, 1.96; 95% confidence interval, 0.98-3.94). Fluconazole had an early and persistent effect on the vaginal mycoflora, with the emergence of C. glabrata vaginal colonization within the first 6 months. The effect of fluconazole prophylaxis can be attributed to the reduction in vaginal C. albicans colonization; however, C. glabrata colonization rapidly supervened.

AIDS-Related Opportunistic Infections↗
PubMed2000

Origin of HIV type 1 in colonial French Equatorial Africa?

Sociocultural factors during the postcolonial period have been implicated as paramount in generating conditions that promoted both the origin and subsequent epidemic spread of HIV-1 in Africa. We suggest, however, that the origin of the disease may lie in the interaction between colonial practices (e.g., labor camps, nonsterile vaccination campaigns) and traditional bushmeat hunting in French Equatorial Africa. Both the epidemiology of HIV-2 and the colonial history of West Africa appear more complex, but similar conditions existed there and may have contributed to the origin of HIV-2. Focusing the search for the origins of HIV-1 and HIV-2 on this earlier time period may contribute to understanding the evolution of the HIV viruses and the dynamics of emerging diseases.

Adaptation, Physiological↗
PubMed2001

Daily interferon therapy for hepatitis C virus infection in liver transplant recipients.

BACKGROUND: Hepatitis C virus infection persists after liver transplantation and causes recurrent liver injury in the majority of patients. Standard dose interferon therapy has been largely unsuccessful for hepatitis C in transplant recipients. METHODS: Twelve patients, at least 7 months posttransplant, with detectable hepatitis C virus RNA in serum and features of hepatitis C on liver biopsy were randomized to interferon-alpha2a, 3 mU daily for 12 months (n=8) or no treatment (n=4). The tolerability of daily interferon dosing in liver transplant recipients was evaluated and effects on hepatitis C virus RNA level, quasispecies evolution, and liver histology were studied. RESULTS: Treated patients had an improvement in histological activity index at the end of therapy relative to controls (median reduction of 2 versus median increase of 1.5) (P=0.04). Four treated patients had a virological response (all bDNA negative, one qualitative polymerase chain reaction negative) compared with none of the untreated patients. Only two of six treated patients tested had evidence of quasispecies diversification on therapy. Seven of eight patients in the treatment group required dose reduction for fatigue and/or depression. They tolerated 1.5 mU of interferon-alpha2a daily. Two treated patients developed graft dysfunction, one of who had histological evidence of rejection and subsequent graft loss. CONCLUSIONS: Low daily doses of interferon were tolerated by liver transplant recipients and provided histological benefit without associated quasispecies diversification in most cases. These findings provide a rationale to study low dose daily or pegylated interferon maintenance therapy for the management of hepatitis C posttransplant.

Adult↗
PubMed2005

HCV infection in very-long-term survivors after cancer chemotherapy and bone marrow transplantation: a single-center experience.

The long-term evolution of hepatitis C virus (HCV) infection in oncologic and/or transplanted patients is still unknown. Patients treated for cancer are different from the general HCV-infected population because of the immunosuppression and the hepatotoxic treatments, which act as co-factors of liver damage. Recently it was observed that antimetabolites play a role in accelerating the process of hepatic fibrosis. The aims of this retrospective study were to describe the clinical course of chronic hepatitis C acquired during anticancer treatment in a group of patients referred to a single center, and to correlate the course of hepatic disease to the type of treatment they received. Among the 17 children who underwent very long follow-up (range 10-18.5 years), the authors identified a group with more active hepatic cytolysis through the serial observation of mean ALT values, HCV RNA determination, and histologic data when available. During follow-up, none of them developed hepatic failure, cirrhosis, or hepatocarcinoma. No single risk factor, such as exposure to antimetabolites, alkylating agents, or other chemotherapy, radiotherapy to the abdomen, exposure to other hepatotoxic drugs, appearance of vaso-occlusive disease, acute and/or chronic graft-versus-host disease, or length of immunosuppression, correlated with a worse course of hepatitis. No definitive conclusions can be drawn. However, multivariate analysis of hepatic risk factors in larger cohorts of patients will be able to provide us with more precise information about the clinical outcome of chronic hepatitis in survivors.

Adolescent↗
PubMed2005

Heart transplantation in patients with chronic hepatitis B: clinical evolution, molecular analysis, and effect of treatment.

We evaluated clinical evolution and hepatitis B virus (HBV) molecular changes in heart recipients with chronic HBV infection before transplantation, and studied the effects of lamivudine treatment in patients who experienced HBV reactivation. Nine patients with chronic HBV infection who underwent heart transplantation were investigated. HBV surface/core-promoter/precore/core regions were sequenced. Prior to transplantation, all nine patients had consistently normal ALT and low HBV-DNA levels. Seven experienced HBV reactivation after transplantation (ALT elevated, HBV-DNA>200.000 cps/ml). Lamivudine treatment was initially effective in all patients; three patients during the second year of treatment developed lamivudine resistance-associated mutations (rt-L180M, rt-M204V) with severe disease reactivation, remitted after switch to adefovir treatment. No other significant HBV mutations were identified in the genomic regions studied. Immune suppression is crucial in the reactivation of previous inactive HBV infection and in the liver disease progression in heart recipients. Preemptive lamivudine treatment could be useful in the early management of these patients.

Adenine↗
PubMed1995

Evolution of the HA1 domain of human influenza A (H1N1) virus: loss of glycosylation sites and occurrence of herald and conserved strains.

Thirty-one strains of human influenza A (H1N1) viruses isolated in Europe, mostly in Finland, from 1978-1992 were compared with respect to their nucleotide sequences coding for the HA1 portion of haemagglutinin. In 1984, at least two sublineages of H1N1 subtype viruses co-circulated in Finland. The viruses isolated after 1986 formed three sequential phylogenetic clusters. Loss of glycosylation sites, on the globular head of the HA1 portion suggests that oligosaccharides at these sites are not necessarily advantageous for the human virus. Isolation of a herald strain in Finland in June 1988 raised the question as to whether the virus was able to survive in Europe throughout the non-epidemic summer period. Demonstration of highly conserved strains, found over two continents in 1988, is further evidence of the existence of infection chains whose viruses have not been subjected to random sampling or selection events.

Amino Acid Sequence↗
PubMed2001

Dynamics of HIV infection: a cellular automata approach.

We use a cellular automata model to study the evolution of human immunodeficiency virus (HIV) infection and the onset of acquired immunodeficiency syndrome (AIDS). The model takes into account the global features of the immune response to any pathogen, the fast mutation rate of the HIV, and a fair amount of spatial localization, which may occur in the lymph nodes. Our results reproduce the three-phase pattern observed in T cell and virus counts of infected patients, namely, the primary response, the clinical latency period, and the onset of AIDS. The dynamics of real experimental data is related to the transient behavior of our model and not to its steady state. We have also found that the infected cells organize themselves into spatial structures, which are responsible for the decrease on the concentration of uninfected cells, leading to AIDS.

Cell Death↗
PubMed1993

Chronic hepatitis in multiple virus infection: histopathological evaluation.

The frequency and histological pattern of multiple hepatitis virus infection was studied in 161 Italian patients who had consecutively undergone liver biopsy from 1989 to 1991. The histological features were compared with that of infection with a single virus. Thirty-nine per cent of patients had evidence of past or present multiple infection, the commonest of which was hepatitis C virus (HCV) in patients with evidence of previous infection with hepatitis B virus (HBV). In general, the severity of the histological pattern of each viral infection was maintained even when more than one virus was involved; there was neither exacerbation nor diminution of the histological changes. The delta-virus (HDV) was not associated with severe necro-inflammatory lesions, but HDV-positive patients were few in this cohort. Lymphoid follicle formation (a putative histological marker of HCV infection) was also found in a high proportion of HCV-negative patients but expressing much HBcAg or HDAg in liver tissue. Possible explanations for this finding are that follicles are relatively non-specific for HCV infection, or that these cases represent HCV infection with false-negative serology. The results of this study suggest that multiple hepatitis virus infection is common in the population investigated and that HBV and HCV co-infection cannot be reliably diagnosed histologically. Whether double infection with these viruses influences the cirrhotic evolution of the liver lesion remains unclear.

Adolescent↗
PubMed1994

Neuropathologic aspects of lentiviral infections.

Studies of lentiviral infections of various animals and man have shown that all may invade the CNS and induce pathological lesions. This is well established in infections with VV, CAEV, SIV, HIV-1, and FIV. Although VV and CAEV do not cause an overt immunodeficiency, they share several features pertinent for the establishment of neuropathologic lesions with those that induce immunodeficiency. This holds especially true for the initial steps and early CNS lesions. 1) Infection of the CNS is from the blood stream. Although a definite proof of how the different viruses cross the blood-brain barrier remains to be brought forward there are indications that it may occur through migration of infected monocytes and/or lymphocytes into the brain. Furthermore free virus may enter the CNS, either directly or through infection of endothelial cells. 2) The lesion pattern at least in initial stages is similar; that is, it consists of meningitis, perivascular infiltrations especially of the deep white matter, and inflammation of the choroid plexus. In visna a local amplification of the inflammatory response is frequently observed in choroid plexus often with formation of active lymphoid follicles. Multinucleated giant cells are prominent in HIV-1 and SIV infections, but rare in VV, and practically nonexistent in infections with FIV and CAEV, possibly a reflection of differences in virus replication. Myelin breakdown is a feature of various lentiviral infections but its mechanisms and morphological expression may vary. Sharply demarcated plaques of primary demyelination seem to be unique for VV infection and vacuolar myelopathy for infection with HIV-1. 3) The main target cells in the brain are cells of the monocyte/macrophage/microglial lineage. In visna infected monocytes are found but evidence for infection of the enigmatic resident microglial cells is still lacking. Infection, especially productive, of neuroectodermal cells is rare, but may, however be important for viral persistence. Infection of endothelial cells occurs in the various lentiviral infections and may play a part in viral entry into the CNS and contribute to tissue damage. 4) The discrepancy between the frequency of productively infected cells and cell types infected and extent and character of pathological lesions, indicates that a mechanism other than the direct effect of the virus contributes to the evolution of CNS lesions. In HIV-1 infection evidence, mainly obtained by in vitro studies, indicates that lesions are mediated by cytokines and other toxic factors secreted by inflammatory or glial cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗