Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Superinfection”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Close association between shape alteration and loss of immunity to superinfection in a wild-type Klebsiella pneumoniae stable lysogen which can be both immune and nonimmune to superinfection.

Klebsiella pneumoniae MirM7 is a wild-type strain which grows as cocci at pH 7 and above and as rods at pH 6.5 and below. Cultures of this strain and an auxotrophic derivative, MirM7b, have been found to undergo spontaneous lysis after purification from possible contaminating viruses. Lysates always contained two phages, FR2 and AP3, most often at high titers. FR2 and AP3 plated with the same efficiency on both MirM7b and K59 (another K. pneumoniae strain sensitive to FR2 and AP3) and lysogenized 45 and 54% of the K59-infected cells, respectively. These findings raise the possibility that MirM7b is lysogenic for FR2 and AP3, although nonimmune to their superinfection. The fact that mitomycin C and N-methyl-N'-nitro-N-nitrosoguanidine can induce phages FR2 and AP3 from MirM7b confirmed this possibility. When MirM7b was infected with FR2 several strains immune to FR2 and AP3, which were all rod shaped, were obtained. Furthermore, 19 derivatives, rod shaped at all pH's have been isolated from MirM7b. They were all immune to both FR2 and AP3. From mating experiments between the MirM7b donor derivative, strain M720, and either K59 or MirCV5, a rod-shaped MirM7b derivative cured from the prophages, cysteine recombinants were obtained which were most often (80%) immune to FR2 and AP3. Nonimmune and still lysogenic recombinants were obtained by mating M720 with a rod-shaped immune MirM7b derivative; the majority of the non-immune strains maintained the rod shape. Five coccus-shaped recombinants were also isolated; they were nonimmune to superinfection. Several physiological properties of strain MirM7b and the other nonimmune coccal recombinants have been studied in comparison with those of the rod-shaped immune derivatives. All of the coccal strains have shown several alterations with respect to the rods. The role of possible derepressed prophage genes in the various physiological alterations of MirM7 is discussed, and the analogies between this system and those of vertebrate cells transformed by proviruses are stressed.

Bacteriophages↗
PubMed2004

Impact of acute hepatitis C virus superinfection in patients with chronic hepatitis B virus infection.

BACKGROUND & AIMS: Superinfection in patients with chronic hepatitis B virus (HBV) infection is not uncommon. Acute hepatitis delta virus (HDV) superinfection is associated with severe and/or progressive liver disease. The natural course following acute hepatitis C virus (HCV) superinfection has not been well studied. The aim of this study was to investigate the impact of acute HCV superinfection. METHODS: The clinical features during acute phase and long-term outcomes of acute HCV superinfection were studied and compared with a cohort of acute HDV superinfection and a matched control group of active chronic hepatitis B. RESULTS: Acute HCV superinfection typically occurs as acute icteric hepatitis. The severity is similar to acute HDV superinfection in that hepatic decompensation developed in 34% of patients, hepatitis failure occurred in 11%, and 10% died. During a follow-up period of 1-21 years, patients with acute HCV superinfection had a significantly higher cumulated incidence of cirrhosis (48% at 10 years) and hepatocellular carcinoma (14% at 10 years, 21% at 15 years, and 32% at 20 years) than acute HDV superinfection or active chronic hepatitis B. Hepatitis B surface antigen (HBsAg) seroclearance occurred earlier in HCV superinfected patients. Continuing hepatitis after HBsAg seroclearance was observed only in HCV superinfected patients. CONCLUSIONS: Acute HCV superinfection in patients with chronic HBV infection is clinically severe during its acute phase. The long-term prognosis following acute HCV superinfection is much worse than that following HDV superinfection or active hepatitis B in terms of continuing hepatitis activity after HBsAg loss and the development of cirrhosis or hepatocellular carcinoma.

Acute Disease↗
PubMed2002

[The effects of hepatitis E virus superinfection on patients with chronic hepatitis B: a clinico-pathological study].

OBJECTIVE: To observe the effect of hepatitis E virus (HEV) superinfection on hepatic lesion and hepatitis B virus (HBV) replication in patients with chronic hepatitis B (CHB). METHODS: Totally 122 patients with CHB were enrolled in this study. They were tested for anti-HEV IgM and IgG in serum, amount of HBV DNA in serum and liver tissue obtained by liver biopsy and HBcAg expression in liver tissue. Other parameters such as ALT, total bilirubin (TBil), albumin (A) and globulin (G), gamma-electrophoretic protein (gamma-EP), prothrombin activity (PTA) were also measured. 21 of the 122 patients (17.2%) were found to have HEV superinfection and the remaining 101 were not. Repeat liver biopsy was performed after 1 year in 7 patients with HEV superinfection and 14 patients without. Moreover, HBV DNA amount in serum from 8 HBeAg negative patients with HEV superinfection were tested dynamically in acute and recovery stage of HEV infection. RESULTS: Comparison of the data from the 21 patients with HEV superinfection and 101 without showed that there was no significant difference in the level of A/G ratio (1.74 +/- 0.50 vs. 1.83 +/- 0.37) and gamma-EP [(24.18 +/- 6.36)% vs. (22.27 +/- 4.59)%, P > 0.05]. However, the level of ALT [(244.61 +/- 81.07) U/L vs. (143.87 +/- 47.69) U/L] and TBil [(88.24 +/- 28.54) micro mol/L vs. (46.16 +/- 17.13) micro mol/L] was significantly higher (P < 0.05), but that of PTA lower in the group with HEV superinfection than in the group without superinfection [(58.57 +/- 17.44)% vs. (72.52 +/- 12.25)%, P < 0.05]. So were the amount of HBV DNA in serum [(5.45 +/- 1.86) copies/ml vs. (6.59 +/- 1.28) copies/ml, P < 0.05] and liver tissue [(6.96 +/- 2.52) copies/g vs. (8.47 +/- 1.79) copies/g, P < 0.05] as well as HBeAg and HBcAg positive rates (8/21 vs. 64/101; 9/21 vs. 67/101, P < 0.05). Pathologically, the hepatic inflammatory activity was more severer in patients with HEV superinfection, but the severity of fibrosis was not significantly different. There was no difference in the severity of inflammatory activity and stage of fibrosis between the 7 patients with HEV superinfection and the 14 patients without as well as before and after 1 year of treatment. The amount of HBV DNA and HBeAg positive rate in serum from recovery stage of HEV infection were higher than those of acute stage. CONCLUSIONS: HEV superinfection leads to activation of hepatic pathological changes and worsens the inflammatory activity. Moreover, HEV superinfection inhibits HBV replication, but it may not be long-lasting.

Adult↗
PubMed1996

Transcriptional effects of superinfection in HIV chronically infected T cells: studies in dually infected clones.

We had previously shown that chronically infected ACH-2 cells (HIVLAI) could be superinfected with HIVRF, that the frequency of superinfection increased with time, and that the transcription of the superinfecting virus exceeded that of the host HIVLAI provirus. In contrast, ACH-2 cells superinfected with a nef-substituted neomycin-resistant (proNEO) provirus were not detectable by DNA polymerase chain reaction (PCR) until geneticin (G418) was added, suggesting that the ability to propagate progressively in culture may be HIV strain specific. Clonal populations of ACH-2 superinfected with proNEO did not demonstrate preferential transcription of the superinfecting virus. However, clones of ACH-2 superinfected with HIVRF (ACH2/RF) showed a preponderance of HIVRF transcripts similar to that seen in bulk populations. Induction of the superinfecting virus by phorbol ester (PMA) occurred more rapidly than the hose provirus and did not equalize transcriptional activity. PCR-derived long terminal repeat (LTR) fragments and Tat cDNAs from A3.01 cells acutely infected with HIVRF or from ACH-2 cells were sequenced and tested for transactivation. The HIVLAI LTR was two to three times more Tat-responsive than the HIVRF LTR. TatRF was two to three times more transcriptionally active on either LTR than TatLAI. Demethylation with 5-azacytidine did not significantly affect HIV expression from the HIVLAI host provirus of superinfected ACH2/RF cell clones. These data suggest that the mechanism of preferential transcription in HIVRF superinfected ACH2/RF may be attributed to the Tat/TAR axis and the effect of the specific locus of host proviral integration.

Amino Acid Sequence↗
PubMed2006

Superinfection of human immunodeficiency virus type 1 (HIV-1) to cell clone persistently infected with defective virus induces production of highly cytopathogenic HIV-1.

Superinfection with human immunodeficiency virus type 1 (HIV-1) in human subjects, defined as reinfection with a heterologous strain of HIV-1, has become a topic of great interest. To illustrate the significance of this occurrence, we performed HIV-1 superinfection of L-2 cells, which were isolated from MT-4 cells persistently infected with subtype B HIV-1 as a cell clone continuously producing defective HIV-1 particles. L-2 cells carrying provirus with a one-base insertion in the pol protease were superinfected with HIV-1 derived from primary isolates of subtype B or CRF01_AE. The kinetics of the superinfection in L-2 were very slow compared with those of primary infections in MT-4. Interestingly, L-2 shifted after superinfection to become a producer of highly cytopathogenic HIV-1. Molecular characterization revealed that superinfection occurred in only about 10% of the CRF01_AE-superinfected L-2, which carried provirus of both subtypes and produced viral particles containing genomic RNA of both subtypes. Surprisingly, such cytopathogenic HIV-1 showed predominantly the original subtype B phenotype. Thus, the mechanism of the production of cytopathic HIV-1 seemed to be mediated by trans complementation with pol products of superinfected CRF01_AE. These findings suggest the significance of long-lived infected cells as recipients for superinfection that could result in the generation of new HIV-1 variants with high virulence in patients who are off therapy or do not adhere to treatment, and may indicate the need for precautions against such superinfection.

Cell Line↗
PubMed2005

Viral reactivation and pseudotype production in an in vitro superinfection system with two different strains of HIV-1.

Viral production and variability of HIV-1 is normally high in vivo causing the necessary conditions for cellular superinfection. In order to evaluate the superinfection dynamics in vitro, H9HTLVIIIB cell line was superinfected with HIVMN. Superinfected cells showed nearly 50% cell mortality at day 1 post-superinfection (ps), which increased significantly up to day 4 ps. Superinfecting genome was detectable until day 10 ps. The superinfecting strain was found in the supernatant only on day 1 ps, but was recovered up to day 4 ps by coculture with non-infected cells. The existing strain (HIVHXB2) was recovered throughout the studied period. Pseudotype formation by the HIVHXB2 genome and envelope proteins of the superinfecting strain (HIVMN) was observed from day 1 to 6 ps. Viral production was increased by 1.7 LOG in superinfected cells from day 1 ps. Both viral production increase and pseudotype formation could be relevant for HIV pathogenesis in vivo.

Cell Line↗
PubMed2006

Risk factors of superinfection following imipenem/cilastatin therapy in hospitalised patients with acute exacerbations of severe chronic obstructive pulmonary disease.

Imipenem is often used in treatment of acute exacerbations of severe chronic obstructive pulmonary disease (COPD). Superinfection following imipenem therapy is a common cause of treatment failure and high economic burden. This study is aimed to explore any clinical factors which determine the risk of superinfection after imipenem treatment in acute exacerbations of severe COPD. A prospective observational study was conducted in a 5-bed respiratory intensive care unit of a Chinese University hospital. Fifty-one patients with acute exacerbations of severe COPD who were hospitalised and treated with imipenem for more than 3 days were enrolled during 1.5 year. The associations between the risk of superinfection and potential factors were analysed by logistic regression. Forty-seven out of 51 patients (92.2%) had their symptoms and signs improved at the end of imipenem treatment. Superinfections were developed in 12 patients, and the superinfection rate was as high as 30.8% (12 out of 39 patients with definite bacteriologic responses). The frequent superinfecting organisms were Stenotrophomonas maltophilia and Pseudomonas aeruginosa. Among a wide range of potential risk factors, we found that lower blood pH, previous cephalosporines treatment and longer period of imipenem treatment are independently associated with a higher risk of superinfection. The risk of superinfection following imipenem treatment in hospitalised patients with acute exacerbations of COPD was high. Lower blood pH, previous cephalosporines treatment and longer period of imipenem treatment all increased the risk of superinfection.

Acute Disease↗
PubMed2005

In-depth analysis of a heterosexually acquired human immunodeficiency virus type 1 superinfection: evolution, temporal fluctuation, and intercompartment dynamics from the seronegative window period through 30 months postinfection.

Human immunodeficiency virus type 1 (HIV-1) superinfection refers to the acquisition of another strain by an already infected individual. Here we report a comprehensive genetic analysis of an HIV-1 superinfection acquired heterosexually. The infected individual was in a high-risk cohort in Tanzania, was exposed to multiple subtypes, and was systematically evaluated every 3 months with a fluorescent multi-region genotyping assay. The subject was identified in the window period and was first infected with a complex ACD recombinant strain, became superinfected 6 to 9 months later with an AC recombinant, and was monitored for >2.5 years. The plasma viral load exceeded 400,000 copies/ml during the first 9 months of infection but resolved to the set point of 67,000 copies/ml by 3 months after superinfection; the CD4 cell count was 377 cells/mul at 30 months. Viral diversity was evaluated with techniques designed to fully sample the quasi-species, permitting direct observation of the evolution, temporal fluctuation, and intercompartment dynamics of the initial and superinfecting strains and recombinants derived from them. Within 3 months of superinfection, seven different molecular forms were detected in gag and six were detected in env. The proportions of forms fluctuated widely over time in plasma and peripheral blood mononuclear cells, illustrating how challenging the detection of dually infected individuals can be. Strain-specific nested PCR confirmed that the superinfecting strain was not present until the 9 month follow-up. This study further defines the parameters and dynamics of superinfection and will foster appropriate studies and approaches to gain a more complete understanding of risk factors for superinfection and its impact on clinical progression, epidemiology, and vaccine design.

Evolution, Molecular↗
PubMed1973

Superinfection exclusion by incomplete genomes of bacteriophage T4.

The genetic basis of superinfection exclusion by bacteriophage T4 was investigated by using incomplete genomes derived from the gene 66 mutant E920g. Incomplete genomes, which included a region of T4 between genes 42 and 44, were able to exclude superinfecting phage with an efficiency similar to that of complete genomes. Those genomes which did not include this region were unable to exclude superinfecting phage. A mutant with reduced ability to exclude super-infecting phage was isolated after mutagenesis with hydroxylamine. The mutation maps midway between amN122 in gene 42 and amB22 in gene 43. The efficiency of exclusion of superinfecting phage (as measured by the percentage of superinfected cells which failed to release any phage carrying selected markers of the superinfecting phage) by this mutant was 50 to 60%, whereas for wild type it was 85 to 95%. Uptake of (3)H-leucine by cells infected with the mutant was inhibited by superinfection with ghosts and it has therefore been designated imm1, for lack of immunity to superinfecting phage and ghosts. The formation of infective centers by cells infected with imm1 or another imm(-) mutant (imm2) was not inhibited by superinfection with ghosts.

Alleles↗
PubMed1971

Breakdown and exclusion of superinfecting T-even bacteriophage in Escherichia coli.

In bacterial strains containing the deoxyribonuclease endonuclease I (endonuclease I(+) strains), 70 to 80% of the injected superinfecting T-even phage deoxyribonucleic acid (DNA) is rapidly degraded to oligonucleotides having an average chain length of 8, the same value as that obtained by endonuclease I digestion of purified T-even phage DNA in vitro. In endonuclease I(-) strains, less than 5% of the injected superinfecting T-even phage DNA is degraded to acid-soluble components. The superinfecting phage DNA is, however, fragmented into a large segment having a molecular weight of about 90 x 10(6) and 30 or more small acid-insoluble segments having molecular weights of less than 10(6). In both endonuclease I(+) and endonuclease I(-) strains, over 80% of the DNA from adsorbed primary T2 or T4 phage, but only 50% of the DNA from adsorbed superinfecting T2 or T4 phage, is injected. Superinfecting T4 are genetically excluded as efficiently from endonuclease I(-) strains as they are from endonuclease I(+) strains. The excluded phage cannot complement defects in either early or late gene functions carried by the primary phage. The induction of both superinfection breakdown and superinfection exclusion requires a period of protein synthesis between primary infection and addition of the superinfecting phage. These observations seem best explained by failure of superinfecting DNA to enter the host cell cytoplasm, presumably as a result of changes in the cell envelope induced by the primary phage.

Centrifugation, Density Gradient↗
PubMed2004

Superinfection following smallpox vaccination (Vaccinia), United States: surveillance January 2003 through January 2004.

BACKGROUND: Superinfection is an adverse event following smallpox vaccination. The clinical presentation is similar to that of a large normal vaccine reaction or "robust take," and the frequency is unknown. METHODS: We retrospectively reviewed all reported severe local reactions consistent with superinfection among United States civilian smallpox vaccinees from January 2003 through January 2004. We applied a standard case definition and estimated the frequency of superinfection following smallpox vaccination. RESULTS: We identified 48 reported cases for further review among 39,350 [corrected] smallpox vaccinees. Two (4%) of the 48 reported cases met the case definition for superinfection; neither of the patients had a pathogenic organism isolated from their infection site. Both were treated with antibiotics and resolved their infection. Of the 46 cases determined not to be superinfection, 41 (89%) were temporally consistent with a large normal vaccine reaction. Thirty (75%) of 40 reported case patients for whom data were available received antibiotic therapy. CONCLUSIONS: Superinfection following smallpox vaccination is rare. Most of the reported superinfection cases were probably large normal smallpox vaccine reactions. Educating providers about the normal response to smallpox vaccine may decrease the overdiagnosis of superinfection and the unnecessary use of antimicrobials.

Adult↗
PubMed2005

HIV drug resistance acquired through superinfection.

OBJECTIVE: HIV interclade B superinfection has previously been described in individuals initially infected with drug resistant virus who then become superinfected by a drug susceptible strain. We report an individual initially infected with a drug-sensitive clade B strain of HIV who was superinfected with another clade B strain resistant to two classes of antiretroviral drugs. METHODS AND DESIGN: To differentiate superinfection from possible co-infection we applied three independent molecular techniques: dye-primer sequencing of a pol fragment, length polymorphism analysis of the V4-5 coding region of the env gene and clonal sequencing of the V3 coding region of the env gene. To assess viral fitness we performed replication capacity assays of the pol gene. RESULTS: These investigations supported the conclusion that this was a case of superinfection and not co-infection. Coincident with acquiring the new strain, the individual's viral load increased by about 10,000 copies/ml with a decrease of 150 x CD4 T cells/mul over the next 6 months. The greater in vivo fitness of the second virus was not supported by the replication capacity assay. Furthermore, superinfection negatively impacted this individual's treatment course. It was not known that he had acquired a drug resistant strain before entering a treatment study, and he had an incomplete response to therapy most likely because the superinfecting viral strain had a decreased susceptibility to two of the prescribed medications. CONCLUSION: HIV drug resistance acquired through superinfection significantly lowers the likelihood of successful antiretroviral therapy and undermines the clinical value of a patient's prior drug resistance testing and lack of prior antiretroviral use.

Adult↗
PubMed1997

Different integrated and unintegrated HIV-1 DNA after superinfection and cell to cell transmission.

Efficient superinfection of H9HTLVIIIB cell line (persistently infected with HIVHXB2 strain) with HIVMN strain is reported. The superinfecting viral DNA was found in the chromosomic and extrachromosomic fractions at early stages, but at 48 hours post superinfection, it remained mainly unintegrated. Interestingly, superinfected cells only produced HIVHXB2 in the supernatant and no increase of viral yield of this persistent virus was observed. Remarkably, virions of both strains. HIVHXB2 and HIVMN, were recovered after cocultivating superinfected cells with MT2 cell line. In the extrachromosomic fractions of seven different superinfected subclons of H9HTLVIIIB, viral DNA of the superinfecting HIVMN strain predominated while in the chromosomic fraction, the proportion of superinfecting viral DNA differed. The study of the presence of different integrated and unintegrated genomes in a single cell could be crucial in the understanding of HIV biology.

Cell Line↗
PubMed1982

The interaction of non-transforming Epstein-Barr virus (EBV) with cell-associated EBV DNA in superinfected lymphoblastoid cell lines.

Two human lymphoblastoid cell lines were established by the transformation of human cord-blood lymphocytes with transforming Epstein-Barr virus (EBV). One cell line (HLB-R1) was established with EBV obtained after the superinfection of Raji cells with HR-1 EBV and the other (HLB-Bl) was established from B95-8 EBV-infected human cord-blood lymphocytes. Both the HLB-R1 and HLB-B1 lines were susceptible to superinfection with HR-1 EBV. We found that EBV DNA was replicated in the superinfected cell lines and that transforming EBV was produced in both the HLB-B1 and HLB-R1 cells. The average titer of transforming EBV obtained in the HR-1 EBV superinfected HLB-B1 and HLB-R1 cell lines was 10(4) transforming units (TU)/ml, whereas the average titers of transforming EBV obtained by the superinfection of Raji cells was 10(1) TU/ml. Epstein-Barr virus capable of inducing early antigen (EA) in superinfected Raji cells (lytic virus) was not detected in any transforming virus preparation. Restriction enzyme digestion patterns of virus DNA isolated from HR-1 and B95-8 cells, as well as from superinfected cells, were compared. The EBV DNA that was replicated in the superinfected HLB-R1 and HLB-B1 cell lines showed a more complex pattern. Our data suggest that recombination between input HR-1 EBV DNA and latent cell-associated EBV DNA occurs. Presumably this recombination results in a change in the biological properties of the newly synthesized virus.

Burkitt Lymphoma↗
PubMed2005

Distinctly different msp2 pseudogene repertoires in Anaplasma marginale strains that are capable of superinfection.

Lifelong persistent infection of cattle is a hallmark of the tick transmitted pathogen Anaplasma marginale. Antigenic variation of Major Surface Protein 2 (MSP2) plays an important role in evasion of the host immune response to allow persistence. Antigenic variation of MSP2 is achieved by gene conversion of pseudogenes into the single operon linked expression site and the diversity of variants is defined by the pseudogene repertoire. Once an animal is persistently infected with one strain of A. marginale, infection with a second strain (superinfection) is rare. However, we recently detected animals superinfected with different strains of A. marginale and hypothesized that the msp2 pseudogene repertoire would be distinct in these superinfecting strains, consistent with encoding different sets of surface variants. Five strains of A. marginale were selected in order to identify and compare msp2 pseudogene content; these included strains with similar and different msp1alpha genotypes, and genotypes that were representative of the strains that were found in the superinfected animals. Southern blot analysis of strains associated with superinfection revealed distinctly different msp2 banding patterns, in contrast to a pattern suggesting identical pseudogene content among related strains not associated with superinfection. Indeed, targeted sequence analysis of msp2 pseudogenes showed identical pseudogene repertoires in genotypically closely related strains and varying amounts of dissimilarity in the pseudogene repertoire in strains with distinctly different msp1alpha genotypes, but totally different msp2 pseudogene repertoires between the strains that were found in superinfected animals. This finding supports the hypothesis that the occurrence of superinfection reflects the differences in the msp2 repertoire and corresponding diversity of variants.

Amino Acid Sequence↗