Talk:Abnormal Development - Human Immunodeficiency Virus
|About Discussion Pages|
Cite this page: Hill, M.A. (2021, January 27) Embryology Abnormal Development - Human Immunodeficiency Virus. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Human_Immunodeficiency_Virus
10 Most Recent SOMS Papers
Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
Fetal Human Immunodeficiency Virus
<pubmed limit=5>Fetal Human Immunodeficiency Virus</pubmed>
HIV-1 Nef Breaches Placental Barrier in Rat Model
PLoS One. 2012;7(12):e51518. doi: 10.1371/journal.pone.0051518. Epub 2012 Dec 11.
Singh P, Agnihotri SK, Tewari MC, Kumar S, Sachdev M, Tripathi RK. Source Toxicology Division, Central Drug Research Institute (Council of Scientific and Industrial Research), Lucknow, Uttar Pradesh, India.
The vertical transmission of HIV-1 from the mother to fetus is known, but the molecular mechanism regulating this transmission is not fully characterized. The fetus is highly protected by the placenta, which does not permit microbial pathogens to cross the placental barrier. In the present study, a rat model was established to observe the effect of HIV-1 protein Nef on placental barrier. Evans blue dye was used to assay permeability of placental barrier and fourteen day pregnant Sprague Dawley rats were injected intravenously with 2% Evans blue dye along with various concentrations of recombinant Nef. After an hour, animals were sacrificed and dye migration was observed through the assimilation of peripheral blood into fetus. Interestingly, traces of recombinant Nef protein were detected in the embryo as well as amniotic fluid and amniotic membrane along with placenta and uterus. Our study indicates that recombinant HIV-1-Nef protein breaches the placental barrier and allows the migration of Evans blue dye to the growing fetus. Further the concentration of Nef protein in blood is directly proportional to the intensity of dye migration and to the amount of Nef protein detected in uterus, placenta, amniotic membrane, amniotic fluid and embryo. Based on this study, it can be concluded that the HIV-1 Nef protein has a direct effect on breaching of the placental barrier in the model we have established in this study. Our observations will be helpful to understand the molecular mechanisms related to this breach of placental barrier by Nef in humans and may be helpful to identify specific Nef inhibitors.
Placental Hofbauer cells limit HIV-1 replication and potentially offset mother to child transmission (MTCT) by induction of immunoregulatory cytokines
Retrovirology. 2012 Dec 5;9:101. doi: 10.1186/1742-4690-9-101.
Johnson EL, Chakraborty R. Source Department of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, GA, 30322, USA. email@example.com.
BACKGROUND: Despite readily detectable levels of the HIV-1 (co)-receptors CD4, CCR5 and DC-SIGN on placental macrophages (Hofbauer Cells [HCs]), the rate of HIV-1 infection in utero in the absence of interventions is only 7% of exposed infants. Here, we examine the replication kinetics of human HCs to the primary isolate HIV-1BaL. We also determined the infectivity of HIV-1-exposed HCs by co-culturing with isolated cord and peripheral blood mononuclear cells [CBMCs, PBMCs]. To understand the limiting nature of HCs to HIV-1 replication, we examined the effect of endogenously secreted cytokines on replication kinetics. RESULTS: HCs have reduced ability to replicate HIV-1 in vitro (p < 0.01) and to transmit virus to CBMCs and PBMCs (p < 0.001 for both) compared to standard infections of MDMs. HCs were shown to release HIV-1 particles at levels comparable to MDMs, however exhibit significant decreases in viral transcription (gag and env), which may account for lower levels of HIV-1 replication. Un-stimulated HCs constitutively express significantly higher levels of regulatory cytokines, IL-10 and TGF-β, compared to MDMs (p < 0.01), which may contribute to immunoregulatory predominance at the placenta and possibly account for down-regulation of HIV-1 replication and infectivity by HCs. We further demonstrate that these regulatory cytokines inhibit HIV-1 replication within HCs in vitro. CONCLUSION: HCs have reduced ability to replicate and disseminate R5-tropic HIV-1BaLin vitro and potentially offset mother to child transmission (MTCT) of HIV-1 by the induction of immunoregulatory cytokines. Despite the potential for migration and infectivity, HCs are not present in the neighboring fetal circulation. These results implicate HCs as important mediators of protection at the feto-maternal interface during ongoing HIV-1 exposure. PMID 23217137
HIV mother-to-child transmission, mode of delivery, and duration of rupture of membranes: experience in the current era
Infect Dis Obstet Gynecol. 2012;2012:267969. doi: 10.1155/2012/267969. Epub 2012 May 28.
Mark S, Murphy KE, Read S, Bitnun A, Yudin MH. Source Department of Obstetrics and Gynecology, University of Toronto, 92 College Street, Toronto, ON, Canada M5G 1L4. firstname.lastname@example.org
OBJECTIVE: To evaluate whether the length of time of rupture of membranes (ROM) in optimally managed HIV-positive women on highly active antiretroviral therapy (HAART) with low viral loads (VL) is predictive of the risk of mother to child transmission (MTCT) of the human immunodeficiency virus (HIV). STUDY METHODS: A retrospective case series of all HIV-positive women who delivered at two academic tertiary centers in Toronto, Canada from January 2000 to November 2010 was completed. RESULTS: Two hundred and ten HIV-positive women with viral loads <1,000 copies/ml delivered during the study period. VL was undetectable (<50 copies/mL) for the majority of the women (167, 80%), and <1,000 copies/mL for all women. Mode of delivery was vaginal in 107 (51%) and cesarean in 103 (49%). The median length of time of ROM was 0.63 hours (range 0 to 77.87 hours) for the entire group and 2.56 hours (range 0 to 53.90 hours) for those who had a vaginal birth. Among women with undetectable VL, 90 (54%) had a vaginal birth and 77 (46%) had a cesarean birth. Among the women in this cohort there were no cases of MTCT of HIV. CONCLUSIONS: There was no association between duration of ROM or mode of delivery and MTCT in this cohort of 210 virally suppressed HIV-positive pregnant women.
Mother-to-child transmission of human immunodeficiency virus in a ten years period
Reprod Health. 2011 Nov 30;8:35. doi: 10.1186/1742-4755-8-35.
Delicio AM, Milanez H, Amaral E, Morais SS, Lajos GJ, e Silva JL, Cecatti JG. Source Department of Obstetrics and Gynecology, School of Medicine, University of Campinas, Brazil. email@example.com
OBJECTIVES: to evaluate mother-to-child transmission (MTCT) rates and related factors in HIV-infected pregnant women from a tertiary hospital between 2000 and 2009. SUBJECTS AND METHOD: cohort of 452 HIV-infected pregnant women and their newborns. Data was collected from recorded files and undiagnosed children were enrolled for investigation. Statistical analysis: qui-square test, Fisher exact test, Student t test, Mann-Whitney test, ANOVA, risk ratio and confidence intervals. RESULTS: MTCT occurred in 3.74%. The study population displayed a mean age of 27 years; 86.5% were found to have acquired HIV through sexual contact; 55% were aware of the diagnosis prior to the pregnancy; 62% were not using HAART. Mean CD4 cell-count was 474 cells/ml and 70.3% had undetectable viral loads in the third trimester. HAART included nevirapine in 35% of cases and protease inhibitors in 55%; Zidovudine monotherapy was used in 7.3%. Mean gestational age at delivery was 37.2 weeks and in 92% by caesarian section; 97.2% received intravenous zidovudine. Use of AZT to newborn occurred in 100% of them. Factors identified as associated to MTCT were: low CD4 cell counts, elevated viral loads, maternal AIDS, shorter periods receiving HAART, other conditions (anemia, IUGR (intra uterine growth restriction), oligohydramnium), coinfecctions (CMV and toxoplasmosis) and the occurrence of labor. Use of HAART for longer periods, caesarian and oral zidovudine for the newborns were associated with a decreased risk. Poor adhesion to treatment was present in 13 of the 15 cases of transmission; in 7, coinfecctions were diagnosed (CMV and toxoplasmosis). CONCLUSION: Use of HAART and caesarian delivery are protective factors for mother-to-child transmission of HIV. Maternal coinfecctions and other conditions were risk factors for MTCT.