Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovirus specific sequences located in the 5' NTR are used to amplify viral RNA by PCR. General primers were selected for the amplification of cardioviruses, including encephalomyocarditis virus (EMCV), mengovirus and Theiler's murine encephalomyelitis virus (TMEV. Additionally, ECHO virus type 22, an atypical enterovirus, could also be detected with the general cardiovirus primers. An internal encephalomyocarditis virus specific probe and a general cardiovirus probe are used to discriminate EMCV from other cardioviruses. The sensitivity of the PCR was determined at 10 pfu after hybridization with an internal oligonucleotide probe. Specificity was tested with a broad range of picornaviruses and other nonrelated RNA and DNA viruses. The applicability of the assay was demonstrated by the detection of TMEV RNA in tissue samples from experimentally-infected mice.
 ...
PMID:Molecular identification of cardioviruses by enzymatic amplification. 751 89

Statistical analyses of RNA folding in 5' nontranslated regions (5'NTR) of encephalomyocarditis virus, Theiler's murine encephalomyelitis virus, foot-and-mouth disease virus, and hepatitis A virus indicate that two highly significant folding regions occur in the 5' and 3' portions of the 5'NTR. The conserved tertiary structural elements are predicted in the unusual folding regions (UFR) for these viral RNAs. The theoretical, common structural elements predicted in the 3' parts of the 5'NTR occur in a cis-acting element that is critical for internal ribosome binding. These structural motifs are expected to be highly significant from extensive Monte Carlo simulations. Nucleotides (nt) in the conserved single-stranded polypyrimidine tract for these RNAs are involved in a distinctively tertiary interaction that is located at about 15 nt prior to the initiator AUG. Intriguingly, the proposed common tertiary structure in this study shares a similar structural feature to that proposed in human enteroviruses and rhinoviruses. Based on these common structural features, plausible base pairing models between these viral RNAs and 18 S rRNA are suggested, which are consistent with a general mechanism for regulation of internal initiation of cap-independent translation.
 ...
PMID:Conserved tertiary structural elements in the 5' nontranslated region of cardiovirus, aphthovirus and hepatitis A virus RNAs. 838 42

Porcine teschoviruses (PTVs) belong to the genus Teschovirus within the family Picornaviridae. Hitherto, PTVs have had 13 serotypes associated with a variety of clinical diseases. The virulent PTV-1 strains were associated with highly fatal, nonsuppurative encephalomyelitis of pigs (Teschen disease) in the 1930-1950s. Today, less virulent Talfan strains of PTV-1 are more widespread, and PTVs have contaminated swine herds worldwide (endemic or enzootic) together with a variety of common swine pathogens (multi-infection status). The aim of this study was to investigate the extent to which PTVs play a role in causing diseases in the field, under the endemic and multi-infection situation, when most pigs in the herds are infected and immune. Based on the fecal-oral model of pathogenesis, a set of 15 organs were collected from 30 culled post-weanling piglets of 4-8 weeks old. For nested RT-PCR targeted on the 5'-NTR, the PTV detection rate was 96.7% (by heads), confirming the endemic status, and infection was most commonly detected in the intestines (averaged 61%) and lymphoid organs (averaged 59%), followed by visceral organs (averaged 37%) and the CNS (different parts varied from 17 to 47%). The correlation of PTVs detected by nested RT-PCR and a histological lesion were analyzed by Chi-square test showing that in the field situation only non-suppurative encephalitis in the caudal part of the brain (P=0.054) may be marginal significantly attributed to infection by PTVs. By genotyping based on partial VP1 sequences, 5 serotypes, namely PTV-1, -4, -6, -7, and -11, were identified, with some animals having two serotypes co-existed in different organs.
 ...
PMID:The role of porcine teschovirus in causing diseases in endemically infected pigs. 2288 31

Coxsackievirus A16 (CV-A16) and enterovirus A71 (EV-A71) are closely related enteroviruses that cause the same hand, foot, and mouth disease (HFMD), but neurological complications occur only very rarely in CV-A16 compared to EV-A71 infections. To elucidate host responses that may be able to explain these differences, we performed transcriptomic analysis and real-time quantitative PCR (RT-qPCR) in CV-A16-infected neuroblastoma cells (SK-N-SH), and the results showed that the radical S-adenosylmethionine domain containing 2 (RSAD2) was the highest upregulated gene in the antimicrobial pathway. Increased RSAD2 expression was correlated with reduced viral replication, while RSAD2 knockdown cells were correlated with increased replication. EV-A71 replication showed no apparent correlation to RSAD2 expressions. Absent in melanoma 2 (AIM2), which is associated with pyroptotic cell death, was upregulated in EV-A71-infected neurons but not in CV-A16 infection, suggesting that the AIM2 inflammasome played a significant role in suppressing EV-A71 replication. Chimeric viruses derived from CV-A16 and EV-A71 but containing swapped 5' nontranslated regions (5' NTRs) showed that RSAD2 expression/viral replication and AIM2 expression/viral replication patterns may be linked to the 5' NTRs of parental viruses. Differences in secondary structure of internal ribosomal entry sites within the 5' NTR may be responsible for these findings. Overall, our results suggest that CV-A16 and EV-A71 elicit different host responses to infection, which may help explain the apparent lower incidence of CV-A16-associated neurovirulence in HFMD outbreaks compared to EV-A71 infection.IMPORTANCE Although coxsackievirus A16 (CV-A16) and enterovirus A17 (EV-A71) both cause hand, foot, and mouth disease, EV-A71 has emerged as a leading cause of nonpolio, enteroviral fatal encephalomyelitis among young children. The significance of our research is in the identification of the possible differing and novel mechanisms of CV-A16 and EV-A71 inhibition in neuronal cells that may impact viral neuropathogenesis. We further showed that viral 5' NTRs may play significant roles in eliciting different host response mechanisms.
 ...
PMID:RSAD2 and AIM2 Modulate Coxsackievirus A16 and Enterovirus A71 Replication in Neuronal Cells in Different Ways That May Be Associated with Their 5' Nontranslated Regions. 2926 72