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Late‐onset Intrauterine growth restriction (IUGR) refers to impaired growth and development of the fetus, characterized by placental morphological abnormalities that affect the fetus's supply of nutrients. Human leukocyte antigen‐G (HLA‐G) is physiologically expressed during pregnancy, but decreased in normal placenta during the last weeks of gestation possibly inducing childbirth. Several viruses involved in congenital infection, such as herpesviruses, exploit HLA‐G expression as an immune‐escape mechanism. To date, despite different congenital herpetic infections having been associated with late IUGR, no direct implication of Human herpesvirus 6 (HHV‐6) infection has been reported. We evaluated HLA‐G expression and HHV‐6 infection in 11 placentas from late‐onset IUGR newborns and 11 placentas from uncomplicated pregnancies by histopathological and immunohistochemistry analysis. We found higher levels of HLA‐G expression and HHV‐6 presence in IUGR placenta samples compared with control placenta samples. We report HHV‐6 staining in IUGR placenta samples, characterized by high HLA‐G expression. These preliminary data suggest a possible involvement of HHV‐6 infection in HLA‐G deregulation that might affect vessel remodeling and prevent the correct pregnancy outcome in the IUGR condition. Highlights: This is a retrospective analysis describing the role of HLA‐G expression and HHV‐6 infection in late‐onset intrauterine growth restriction (IUGR) placenta samples.For the first time it has been suggested a possible involvement of HHV‐6 infection in HLA?G deregulation that might affect vessel remodeling and prevent the correct pregnancy outcome in the IUGR condition. [ABSTRACT FROM AUTHOR]

The article offers information on the efficacy of personal protective equipment and hydrogen peroxide (H2O2)-based spray against coronavirus in dental setting. It mentions that efficiency of a hydrogen peroxide-based spray in reducing a coronavirus viral load, similar to that of asymptomatic patients, dispersed during a conventional dental procedure.

On the contrary, Haas et al.[6] failed to detect HPV-positive biopsy specimens in a patient with a 9-year history of generalized eruptive KA of the Grzybowski type. Isolation of DNA was performed as previously described.[7] We avoided specimen contamination by keeping the DNA extraction area strictly separated from the PCR mixture preparation and sample handling. HPV DNA presence was determined using a nested PCR as previously described.[8] HPV-16 DNA presence was determined using a nested PCR specific for HPV-16-E6 region that we set up within the original amplicon published by Ferre and Garduno[12] and a nested PCR with degenerate primers already described by de Roda Husman et al.[13]. [Extracted from the article]

Objectives Inherited chromosomally integrated human herpesvirus-6 (ci HHV-6) is characterised by the complete HHV-6 genome integration into the host germ line genome and is vertically transmitted with a Mendelian inheritance. By now, the only relationship between ci HHV-6 and diseases seems to be with angina pectoris. Methods We report a case of an 82-year-old man diagnosed with diffuse large B-cell lymphoma ( DLBCL) on October 2014. To substantiate the suspicion of ci HHV-6, we analysed peripheral blood mononuclear cells, bone marrow biopsy and pleural effusion-derived mesothelial cells with PCR, RT- PCR and FISH. Results Virological routine screening by PCR showed the absence of HHV-8 and EBV infections, while the presence of HHV-6 DNA (ie, U22, U42 and U94 HHV-6 genes), with a viral load of about 1.0 genome per cell, strongly suggests ci HHV-6. The RT- PCR showed the positivity only for the immediate-early U94, at low levels of transcription (100±15 transcripts/1 μg RNA). FISH analysis reported a case of inherited ci HHV-6 in 17p chromosome region and, for the first time, in a marker chromosome. Conclusions This is the first case of inherited ci HHV-6 in a marker chromosome, possibly elucidating the role of this abnormality in the biology of DLBCL. [ABSTRACT FROM AUTHOR]

Aims: To evaluate (i) the presence of human herpesvirus 7 (HHV-7), Epstein–Barr virus (EBV) and human cytomegalovirus (HCMV), and (ii) the transcription pattern of HHV-7 in gingival biopsies from patients affected by periodontitis (P) and periodontally healthy subjects (H). Material and Methods: Thirty-seven subjects (P: n=24; H: n=13) were included. Each P patient contributed two gingival biopsies (representative of a clinically affected and non-affected site) and each H subject contributed one gingival biopsy. After DNA extraction, nested polymerase chain reaction was used to identify the viruses. Results: HHV-7 was detected in 91.7% of P patients and in 61.5% of H subjects ( p=0.02), EBV in 50.0% samples of P patients and 7.7% of H subjects ( p=0.005) and HCMV only in one sample from H group. EBV was more frequently detected in biopsies from affected sites (50.0%) than from non-affected sites (16.7%) ( p=0.008). HHV-7 transcription was detected in 15.4% of affected and 15.4% of non-affected sites. Conclusions: The results indicate that (i) gingival tissues can be considered a potential reservoir for HHV-7; (ii) when present, HHV-7 persists in a latent state in the majority of cases; (iii) the presence of EBV seems to be associated with the diseased state of the patient and site. [ABSTRACT FROM AUTHOR]

Problem: We first reported human herpesvirus (HHV)‐6A DNA presence in 43% of endometrial cells from women with idiopathic infertility, whereas no fertile control women harbored the virus. We investigated the effect of HHV‐6A infection on the immunological status of the endometrium. Method of study: Endometrial biopsies, uterine flushing, and whole blood samples were collected from 67 idiopathic infertile women (mid‐secretory phase). We analyzed the endometrial immunological status evaluating: (a) the effect of HHV‐6A infection on endometrial immune profile analyzing the ratio of interleukin (IL)‐15/ fibroblast growth factor‐inducible 14 (Fn‐14) and IL‐18/ TNF‐related weak inducer of apoptosis (TWEAK) mRNA as a biomarker of endometrial (e)natural killer activation/maturation, angiogenesis, and Th1/Th2 balance; (b) endometrial receptivity to trophoblasts in endometrial 3D in vitro model; (c) natural killer (NK) cells and T cells percentage and subpopulations by flow cytometry. Results: We confirmed the presence of HHV‐6A infection in a 40% of idiopathic infertile women, characterized by an immune profile reflecting eNK cell cytotoxic activation and a decrease in CD4+ CD25+ CD127dim/− regulatory T cells. The co‐culture of endometrial epithelial cells with spheroids generated from the extravillous trophoblast‐derived cell line JEG3 showed a twofold expansion of spheroids on endometrial epithelial‐stromal cells (ESC) culture surface from HHV‐6A negative women while no expansion was observed on the surface of ESC from HHV‐6A positive women. Conclusion: The identification of an effect of HHV‐6A infection on endometrial immune status opens new perspectives in idiopathic infertile women care management. In addition, it would be possible to select antiviral therapies as novel, non‐hormonal therapeutic approaches to those idiopathic infertile women characterized by the presence of endometrial HHV‐6A infection, to increase their pregnancy rate. [ABSTRACT FROM AUTHOR]