Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Foot-and-mouth disease virus (FMDV) can cause transplacental infection and death in fetal lambs. This study investigates the pathogenesis of FMDV infection in ovine fetuses using in-situ hybridization (ISH) to detect viral transcripts in tissue and real-time reverse transcriptase polymerase chain reaction (RT-PCR) assays to quantify the fetal cytokine response to infection. FMDV ribonucleic acid (RNA) was localized mainly to the heart and skeletal muscles of fetuses and was only occasionally expressed in the lingual epithelium, demonstrating that FMDV has a different tissue tropism in the fetus compared with that in adult sheep. There was early expression of genes encoding anti-viral cytokines (IFN-alpha and IFN-beta) in fetuses at 2 and 4 days post-infection (dpi), followed by a marked rise in the transcription of pro-inflammatory cytokine genes (IFN-gamma, TNF-alpha and IL-1alpha) from 7 to 18 dpi, particularly in the heart. The degree of cytokine mRNA expression correlated with fetal infection and was likely to be a factor in fetal death. In contrast, cytokine gene expression in infected neonatal lambs was much less and mainly occurred between 2 and 4 dpi. This study identifies two key factors in the pathogenicity of FMDV in fetal lambs: viral tropism for cardiac and skeletal muscles, and a marked cytokine response following infection.
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PMID:Foot-and-mouth disease virus infection in fetal lambs: tissue tropism and cytokine response. 1829 84

We investigated the protective potential of recombinant his-tagged antigens recNcMIC1, recNcMIC3 and recNcROP2, applied either as single vaccines or as vaccine combinations, in BALB/c mouse models for cerebral and fetal infection. Subsequently, mice were mated and challenged by i.p. inoculation of 2 x 10(6)Neospora caninum tachyzoites at day 7 of pregnancy. The mortality and morbidity of adult mice (non-pregnant and dams) and of the newborn pups was studied for a period of 40 days following birth. Vaccination of non-pregnant mice with recNcROP2 or combinations of recNcROP2 with recNcMIC antigens significantly reduced the numbers of mice suffering from clinical signs, and morbidity was completely prevented with the combination of all three antigens. Of the dams, the groups receiving either recNcROP2 alone or the combination of all three antigens did not exhibit any morbidity, the groups receiving ROP2 mixed with either MIC1 or MIC3 exhibited reduced numbers of deaths, and in the infection control group and the adjuvant group 50% and 43% of mice, respectively, succumbed to disease. For pups, the highest survival rates were noted for the groups receiving recNcROP2 (50%) and recNcROP2/NcMIC1/NcMIC3 (35%), while in the infection- and adjuvant- control groups all pups died, the latest at days 25 and 30, respectively. Quantification of parasite DNA by N. caninum-specific real-time PCR revealed consistently lower parasite burdens in brain tissue of pups from vaccinated groups compared with the controls. However, dense granule antigen 2 (GRA2) real-time reverse transcriptase-PCR on brain tissue of surviving pups (applied here to detect viable parasites) demonstrated that only the pups from the group vaccinated with all three antigens in combination appeared free of viable tachyzoites, while in all other groups viable parasites were still present. Serological analysis of humoral (total IgG, IgG1 and IgG2a) and serum cytokine (IL-4 and IFN-gamma) responses showed that this effect was associated with a Th-2-biased immune response, with a clearly elevated IL-4/IFN-gamma ratio in the mice receiving all three antigens in combination. In conclusion, a mixture of recombinant antigens representing important secretory micronemal and rhoptry proteins leads to a significant protection against vertical transmission of N. caninum in mice.
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PMID:Vaccination with recombinant NcROP2 combined with recombinant NcMIC1 and NcMIC3 reduces cerebral infection and vertical transmission in mice experimentally infected with Neospora caninum tachyzoites. 1944 10

In utero transmission of feline immunodeficiency virus (FIV) occurs frequently in queens experimentally infected with FIV-B-2542 and other FIV isolates. Fetal infection has been detected as early as 3-4 weeks gestation, and the incidence of fetal infection increases with progressing gestation. Reproductive failure occurs commonly, including fetal resorptions and developmentally-arrested fetuses, demonstrating that fetal demise occurs early in gestation. Precise, temporal immunomodulation within the placenta is essential for successful pregnancy. Placental Th1 and Th2 cytokines must be appropriately balanced, typically favoring Th2 cytokines at the maternal-fetal interface. Abnormal inflammatory cytokine expression often accompanies miscarriage. Regulatory T cells (Tregs) play an essential role in maternal tolerance of the semi-allogeneic fetus by suppressing inflammation. We are using the FIV-infected cat to examine the relationship between lentivirus-induced placental immunopathology and reproductive outcome. Using TaqMan real time reverse transcriptase (RT)-PCR, we measured relative expression of key immunomodulators in the placentas of FIV-B-2542-infected and control cats, including placentas from both viable and nonviable pregnancies. Our data associate significantly-increased expression of inflammatory cytokines with failed pregnancies, identify Treg markers in the placentas, and provide preliminary evidence that Tregs or other cells bearing similar activation markers may be involved in pregnancy maintenance. Our data suggest that placental inflammation in the FIV-infected cat may compromise pregnancy.
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PMID:Placental immunopathology in the FIV-infected cat: a role for inflammation in compromised pregnancy? 1989 19

Rubella is generally a mild and self-limited disease in children. During pregnancy, rubella can have potentially devastating effects on the developing fetus. Postnatal rubella is transmitted primarily by inhalation of virus-laden airborne droplets or direct contact with infected nasopharyngeal secretions. In susceptible pregnant women, the virus may cross the placenta and spread through the vascular system of the developing fetus. Postnatally acquired rubella typically begins with fever and lymphadenopathy, followed by an erythematous, maculopapular rash. The rash classically begins on the face, spreads cephalocaudally, becomes generalised within 24 hours, and disappears within 3 days. Maternal rubella, especially during early pregnancy, may lead to miscarriage, intrauterine fetal death, premature labour, intrauterine growth retardation, and congenital rubella syndrome. Cataracts, congenital heart defects, and sensorineural deafness are the classic triad of congenital rubella syndrome and they typically occur if the fetal infection occurs in the first 11 weeks of gestation. Laboratory confirmation of rubella virus infection can be based on a positive serological test for rubella-specific immunoglobulin M antibody; a four-fold or greater increase in rubella-specific immunoglobulin G titres between acute and convalescent sera; or detection of rubella virus RNA by reverse transcriptase-polymerase chain reaction. Treatment is mainly symptomatic. Universal childhood immunisation and vaccination of all susceptible patients with rubella vaccine to decrease circulation of the virus are cornerstones to prevention of rubella and, more importantly, congenital rubella syndrome.
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PMID:Rubella (German measles) revisited. 3096 19