Disease relevance of Superinfection

• Xanthomonas maltophilia superinfections occurred only in patients receiving imipenem (3 of 135 patients compared with 0 of 268 patients; P = 0.03) [1].
• The SU-AmB-1 line, derived from a patient with low serum antibody titers to Epstein-Barr virus (EBV), was devoid of EBV genomes by the reaction for EBV-associated nuclear antigen (EBNA), could not be induced to express EBV antigens, and was highly refractory to EBV superinfection [2].
• If the CD4 protein is expressed, superinfection can take place, and phenotypically mixed virus particles are produced [3].
• To isolate NeoR-MPSV mutants that are efficiently expressed in PCC4 cells, G418-resistant PCC4 cell lines were induced to differentiate, and the provirus was rescued by superinfection with murine leukemia virus [4].
• Two of the four patients with HCC had a superinfection with hepatitis C virus (HCV) [5].

Psychiatry related information on Superinfection

• Infection of mice with an attenuated Creutzfeldt-Jakob disease agent (SY-CJD) interferes with superinfection by a more virulent human-derived CJD agent (FU-CJD) and does not require pathological prion protein (PrPres) [6].

High impact information on Superinfection

• Superinfection of Ha-MSV-infected cells with A-MuLV overrides their Epo-dependency [7].
• In converted tk+ cells, the fused thymidine kinase gene, like the wild-type gene, is stimulated by superinfection with the tk- virus [8].
• The T antigen-negative, virus rescue-negative clones can be retransformed by superinfection and appear to have lost a considerable proportion of integrated viral DNA sequences [9].
• Enterococcal superinfection in paediatric oncology patients treated with imipenem [10].
• Superinfection with rifampin-isoniazid-streptomycin-ethambutol (RISE)-resistant tuberculosis in three patients with AIDS: confirmation by polymerase chain reaction fingerprinting [11].

Chemical compound and disease context of Superinfection

• Enterococcal superinfection and colonization after therapy with moxalactam, a new broad-spectrum antibiotic [12].
• Production of the virus was not suppressed by 3'-azido-3'-deoxythymidine (AZT), indicating that viral production was not caused by superinfection [13].
• Five patients treated with ampicillin-tobramycin, and none treated with cefotaxime developed superinfections (p = 0.024) [14].
• Streptococcal superinfections developed in three patients (14.2%) in the aztreonam group [15].
• EBV-early antigen induction by superinfection was resistant to inhibition by indomethacin and indicates that induction by chemical inducers and by super-infection follows different pathways [16].

Biological context of Superinfection

• For example, induction of latent HIV-1 gene expression in response to superinfection by herpes simplex virus type 1 (HSV-1) or cytomegalovirus is thought to be mediated, in part, by factors binding the CP2 site [17].
• Following HSV-1 superinfection of transfected HeLa cells, the US11 promoter in ORI+ plasmids was expressed with similar kinetics to the viral US11 promoter [18].
• These results demonstrate that MCF13 MLV induces apoptosis preferentially in cells in which superinfection occurs, and the mechanism involved is independent of p53 activation and mitochondrial damage [19].
• Reporter gene expression was observed in different eukaryotic cell lines following transfection and subsequent superinfection with CCHF virus, confirming encapsidation, transcription, and replication of the pol I-derived minigenomes [20].
• These findings indicate that T-cell killing is a consequence of superinfection and that the mutations in env critical to pathogenicity of the immunosuppressive variant result in a failure to establish superinfection interference in infected cells [21].

Anatomical context of Superinfection

• Enterococcal superinfections occurred in both groups (a bacteremic urinary tract infection in a ceftazidime patient and osteomyelitis in a ciprofloxacin patient) [22].
• Interestingly, these BL/VL3 RadLV-infected nonpermissive fibroblasts were resistant to superinfection by fibrotropic Moloney MuLV, and this resistance also occurred at a late step of the Moloney virus cycle [23].
• In contrast, only 60 times more RNA than DNA was present in virus particles produced by transfection of Jurkat cells, which were CD4-positive and thus potentially susceptible to superinfection [24].
• Epstein-Barr (EB) virus induces a new pyrimidine deoxynucleoside kinase [thymidine kinase (dTk)] activity in Raji B lymphocyte cells after superinfection [25].
• During schistosomiasis, interleukin-5 (IL-5)-dependent eosinophil responses have been implicated in immunopathology, resistance to superinfection, synergistic interactions with chemotherapeutic agents, and the inductive phase of the egg-induced Th2 response [26].

Gene context of Superinfection

• Prior to superinfection, the cells express neither IL-9 nor IL-9R [27].
• AAV2 superinfection of HPV type 31b (HPV31b)-positive cells at early times postinfection resulted in degradation of the cyclin-dependent kinase (CDK) inhibitor p21(WAF1) protein in a proteosome-dependent manner [28].
• Infection of normal MEFs, Hep2, or A549 cells with an adenovirus vector expressing a dominant-negative (DN) IkappaBalpha, followed by superinfection with HSV, resulted in a 98% drop in virus yield [29].
• Consequently, the CD4 CDR3-related region could play a major role as the receptor for the superinfection reported here [30].
• The superinfection exclusion gene (sieA) of bacteriophage P22: identification and overexpression of the gene and localization of the gene product [31].

Analytical, diagnostic and therapeutic context of Superinfection

• In one patient a superinfection with Pseudomonas aeruginosa developed after treatment with ticarcillin plus clavulanate potassium [32].
• Moreover, emergence of resistance accounted for 5 of 9 patients with treatment failure, superinfection, or both when piperacillin was used as a single agent, compared with 2 of 10 similar patients in the combination group (P = 0.1299 by Fisher's exact test) [33].
• In the cefepime group, one death occurred, contributed to by an enterococcal superinfection acquired during study drug therapy, and there were two mild and transient adverse experiences observed [34].
• 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 [35].
• When analysed by the fluorescent antibody technique on smears of methanol fixed parasitized erythrocytes, reinfection and superinfection sera were almost totally cross-reactive both within and across species [36].

References