Carriage of herpes simplex virus and human papillomavirus in oral mucosa is rare in young women: A long-term prospective follow-up

Herpes simplex and human papilloma virus coinfections in oral mucosa of men—A 6‐year follow‐up study

“…HSV‐1 and ‐2 DNA detection was done with a quantitative real‐time PCR using Rotor‐Gene Q real‐time instrument (Qiagen, Hilden, Germany), as described before . Primer and probe sequences for HSV‐1 and ‐2 were derived from the glycoprotein D (gD) gene, as previously described …”

“…Our previous study was the first to evaluate HSV‐1 and HPV DNA co‐infection in oral mucosa sampled by Cytobrush® (MedScan, Malmö, Sweden), in a longitudinal setting. The results showed that HSV‐1 and HPV coinfection in oral mucosa of young women was rare, being found only in 4 (0.2%) samples . This finding was important from clinical point of view, because a recent study showed that head and neck carcinomas (HNSCC) coinfected with HPV16 and HSV‐1 had the least favorable outcome .…”

“…We have recently analyzed oral mucosal samples of 304 healthy women followed for 6 years at pre‐set sampling times. Altogether, 2.2% of all the 1873 collected oral epithelial brush samples were HSV‐1 DNA positive . The shedding into saliva is expected to be more prevalent in immunocompromized patients or in patients with oral surgery …”

Topical Treatment of Herpes Simplex virus Infection with Enzymatically Created siRNA Swarm

“…Herpes simplex virus (HSV) is a ubiquitous human pathogen. Approximately half of the population carries the virus [1][2][3] and 2-5% of individuals are shedding HSV at a given time [4,5]. Cold sores are a common clinical symptom of HSV infection.…”

Herpetic Encephalitis during Pregnancy: Case Report

“…Lesions from primary infections typically resolve after an average of three weeks. 1,[3][4][5][6][7] If vaginal delivery occurs during an active infection, the risk of neonatal transmission increased and thus cesarean delivery is preferred in such cases. 4,[8][9][10][11] Neuronal damage evident in HSE is not well understood, but is thought to be due to the capability of HSV-1 to induce cell death, a property not characteristic of HSV-2.…”