scholarly journals Human papillomavirus and herpes simplex virus infections in patients with mucocutaneous lesions can be linked to host TBX-21 gene polymorphism

2021 ◽  
Vol 25 (3) ◽  
pp. 666-674
Author(s):  
Amin Bakir
Keyword(s):  
Human Papillomavirus ◽  
Herpes Simplex ◽  
Gene Polymorphism ◽  
Hpv Infection ◽  
Virus Infections ◽  
Gene Variation ◽  
Hpv Genotypes ◽  
Simplex Virus ◽  
The Impact ◽  
Hsv 1

Background and objective: Human papillomavirus (HPV) and herpes simplex-2 (HSV-2) are the common cause of genital lesions in women. The variation in host genetic makeup can determine the consequence of a viral infection in that host. T-bet gene polymorphism has been associated with the incidence of several types of infections. This study investigates the impact of T-bet polymorphism on the incidence of HPV and HSV in genital lesions. Methods: 215 women, including 71 HPV infected, 72 HSV-2 infected, and 72 controls were enrolled. Viral genotyping was done on genital swab samples using Realtime PCR. In all participants, the extracted DNA from blood was tested for T-bet gene variation at Ch17.rs17244587 G>A site using ARMS-PCR. ELISA was done to participants sera to detect HSV-1 IgM. Results: Genotyping of HPV infection revealed that (73.0%) were at low risk. Most individuals (72.5%) were homozygous GG, while (20.9%) were heterozygous AG and (6.5%) were homozygous AA, of which 92.8% were HSV-2 infected patients. None of 18 (8.4%) HSV-1-IgM positive women were homozygous AA. Conclusion: T-bet gene allele A appears to be linked with more incidence of HSV-2 in genital lesions, but such influence was not observed for HPV genotypes and HSV-1. Keywords: HPV genotypes; HSV-2 infection; Genital lesion; T-bet polymorphism.

Human papillomavirus, cytomegalovirus and herpes simplex virus infections for cervical cancer in Taiwan

1997 ◽  
Vol 120 (2) ◽  
pp. 217-221 ◽  
Author(s):  
Chih-Ping Han ◽  
Yeou-Ping Tsao ◽  
Chien-An Sun ◽  
Heung-Tat Ng ◽  
Show-Li Chen
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Infections ◽  
Simplex Virus

Essential Oils for the Treatment of Herpes Simplex Virus Infections

Chemotherapy ◽  
2019 ◽  
Vol 64 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Paul Schnitzler
Keyword(s):  
Clinical Trials ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Essential Oils ◽  
Full Potential ◽  
Virus Infections ◽  
Synthetic Drugs ◽  
Cell Adsorption ◽  
Simplex Virus ◽  
Hsv 1

Infections with herpes simplex virus type (HSV)-1 and HSV-2 are distributed worldwide. Although standard therapies with acyclovir and other synthetic drugs are available, the safety and efficacy of these drugs are limited due to the development of drug resistance and adverse side effects. The literature on essential oils and isolated compounds was reviewed regarding their antiviral activities against HSV-1 and HSV-2. The present overview aims to review experimental data and clinical trials focusing on the antiviral activity of selected essential oils and isolated oil components. HSV was found to be susceptible to many essential oils and their constituents. Whereas some essential oils and compounds exhibit direct virucidal activity or inhibit intracellular replication, many essential oils and compounds interact with HSV particles thereby inhibiting cell adsorption. Ayclovir-resistant HSV strains are also susceptible to essential oils since their mode of action is different from the synthetic drug. There are numerous publications on the antiherpetic activity of essential oils and their isolated active compounds. This field of research is still growing, and more clinical trials are required to explore the full potential of different essential oils for the topical treatment of herpetic infections.

scholarly journals Endocytic Internalization of Herpes Simplex Virus 1 in Human Keratinocytes at Low Temperature

2020 ◽  
Author(s):  
Nydia De La Cruz ◽  
Dagmar Knebel-Mörsdorf
Keyword(s):  
Plasma Membrane ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Low Temperature ◽  
Human Keratinocytes ◽  
Herpes Simplex Virus 1 ◽  
Successful Infection ◽  
Simplex Virus ◽  
The Impact ◽  
Hsv 1

Herpes simplex virus 1 (HSV-1) can adopt a variety of pathways to accomplish cellular internalization. In human keratinocytes representing the natural target cell of HSV-1, both direct plasma membrane fusion and endocytic uptake have been found. The impact of either pathway in successful infection, however, remains to be fully understood. To address the role of each internalization mode, we performed infection studies at low temperature as a tool to interfere with endocytic pathways. Interestingly, successful HSV-1 entry in primary human keratinocytes and HaCaT cells was observed even at 7°C, although delayed compared to infection at 37°C. Moreover, ex vivo infection of murine epidermis demonstrated that virus entry at 7°C is not only accomplished in cultured cells but also in tissue. Control experiments with cholera toxin B confirmed a block of endocytic uptake at 7°C. In addition, uptake of dextran by macropinosomes and phagocytic uptake of latex beads was also inhibited at 7°C. Infection of nectin-1-deficient murine keratinocytes affirmed that the entry at 7°C was receptor-dependent. Strikingly, the lysosomotropic agent, ammonium chloride, strongly inhibited HSV-1 entry suggesting a role for endosomal acidification. Ultrastructural analyses in turn revealed free capsids in the cytoplasm as well as virus particles in vesicles after infection at 7°C supporting both plasma membrane fusion and endocytic internalization as already observed at 37°C. Overall, entry of HSV-1 at 7°C suggests that the virus can efficiently adopt nectin-1-dependent unconventional vesicle uptake mechanisms in keratinocytes strengthening the role of endocytic internalization for successful infection. IMPORTANCE The human pathogen herpes simplex virus 1 (HSV-1) relies on multiple internalization pathways to initiate infection. Our focus is on the entry in human keratinocytes, the major in vivo target during primary and recurrent infection. While antivirals reduce the severity of clinical cases, there is no cure or vaccine against HSV. To develop strategies that interfere with virus penetration, we need to understand the various parameters and conditions that determine virus entry. Here, we addressed the impact of virus internalization via vesicles by blocking endocytic processes at low temperature. Intriguingly, we detected entry of HSV-1 even at 7°C which led to infection of primary keratinocytes and epidermal tissue. Moreover, electron microscopy of human keratinocytes at 7°C support that internalization is based on fusion of the viral envelope with the plasma membrane as well as vesicle membranes. These results provide novel insights into conditions that still allow endocytic internalization of HSV-1.

scholarly journals Herpes Simplex Virus Type 1 Neuronal Infection Triggers the Disassembly of Key Structural Components of Dendritic Spines

2021 ◽  
Vol 15 ◽  
Author(s):  
Francisca Acuña-Hinrichsen ◽  
Adriana Covarrubias-Pinto ◽  
Yuta Ishizuka ◽  
María Francisca Stolzenbach ◽  
Carolina Martin ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cortical Neurons ◽  
Neuronal Cell ◽  
Simplex Virus ◽  
The Impact ◽  
Hsv 1

Herpes simplex virus type 1 (HSV-1) is a widespread neurotropic virus. Primary infection of HSV-1 in facial epithelium leads to retrograde axonal transport to the central nervous system (CNS) where it establishes latency. Under stressful conditions, the virus reactivates, and new progeny are transported anterogradely to the primary site of infection. During the late stages of neuronal infection, axonal damage can occur, however, the impact of HSV-1 infection on the morphology and functional integrity of neuronal dendrites during the early stages of infection is unknown. We previously demonstrated that acute HSV-1 infection in neuronal cell lines selectively enhances Arc protein expression - a major regulator of long-term synaptic plasticity and memory consolidation, known for being a protein-interaction hub in the postsynaptic dendritic compartment. Thus, HSV-1 induced Arc expression may alter the functionality of infected neurons and negatively impact dendritic spine dynamics. In this study we demonstrated that HSV-1 infection induces structural disassembly and functional deregulation in cultured cortical neurons, an altered glutamate response, Arc accumulation within the somata, and decreased expression of spine scaffolding-like proteins such as PSD-95, Drebrin and CaMKIIβ. However, whether these alterations are specific to the HSV-1 infection mechanism or reflect a secondary neurodegenerative process remains to be determined.

Frequency of herpes simplex virus, cytomegalovirus and human papillomavirus DNA in semen

2002 ◽  
Vol 13 (8) ◽  
pp. 547-550 ◽  
Author(s):  
Olivier Aynaud ◽  
Jean-Dominique Poveda ◽  
Bernard Huynh ◽  
Aline Guillemotonia ◽  
Renzo Barrasso
Keyword(s):  
Human Papillomavirus ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Hpv Infection ◽  
Hpv Dna ◽  
Associated Lesions ◽  
History Of ◽  
Infected Cells ◽  
Simplex Virus ◽  
Pcr Techniques

Herpes simplex virus (HSV-2) and cytomegalovirus (CMV) infections produce brain damage in the newborn, and human papillomavirus (HPV) plays a role in cervical carcinogenesis. To assess the frequency of herpes virus and HPV in semen and its role in transmission, semen from 111 male partners of women with histologically-detected genital HPV infection was analysed for HSV, CMV and HPV infection. We used cell culture to detect HSV and CMV, and polymerase chain reaction (PCR) for HPV. Virological findings in the sperm were correlated to the presence or absence of HPV-associated genital lesions and to the viral type. Viral cultures yielded HSV-2 DNA in 9% and CMV DNA in 6.3% of cases. No correlation was established with a history of clinically apparent infection for HSV. HPV-DNA was detected in 23.4% of semen by PCR techniques: in 48% of subjects with urethral lesions, in 22% of patients with penile lesions, in 2% of patients without HPV-associated lesions. HPV-DNA type 16 was detected in 3.6% of cases. Patients with a positive HPV semen sample and penile or urethral lesions had the same HPV type detected in the two specimens. The study shows a high detection of clinically inapparent HSV and CMV, but does not confirm high HPV prevalence in semen from men without detectable lesions. Our study also suggests that the mechanism for semen contamination by HPV is the exfoliation of infected cells from urethral lesions during semen ejaculation, and probably, by abrasion from penile lesions. This could result in the contamination of semen used in assisted reproductive technology.

scholarly journals Mucosal Herpes Immunity and Immunopathology to Ocular and Genital Herpes Simplex Virus Infections

2012 ◽  
Vol 2012 ◽  
pp. 1-22 ◽  
Author(s):  
Aziz Alami Chentoufi ◽  
Lbachir BenMohamed
Keyword(s):  
Herpes Simplex ◽  
Virus Infections ◽  
Viral Pathogens ◽  
Herpes Simplex Viruses ◽  
Cold Sores ◽  
Simplex Virus ◽  
Disseminated Disease ◽  
Hsv 1

Herpes simplex viruses type 1 and type 2 (HSV-1 and HSV-2) are amongst the most common human infectious viral pathogens capable of causing serious clinical diseases at every stage of life, from fatal disseminated disease in newborns to cold sores genital ulcerations and blinding eye disease. Primary mucocutaneous infection with HSV-1 & HSV-2 is followed by a lifelong viral latency in the sensory ganglia. In the majority of cases, herpes infections are clinically asymptomatic. However, in symptomatic individuals, the latent HSV can spontaneously and frequently reactivate, reinfecting the muco-cutaneous surfaces and causing painful recurrent diseases. The innate and adaptive mucosal immunities to herpes infections and disease remain to be fully characterized. The understanding of innate and adaptive immune mechanisms operating at muco-cutaneous surfaces is fundamental to the design of next-generation herpes vaccines. In this paper, the phenotypic and functional properties of innate and adaptive mucosal immune cells, their role in antiherpes immunity, and immunopathology are reviewed. The progress and limitations in developing a safe and efficient mucosal herpes vaccine are discussed.

scholarly journals Entry Mechanisms of Herpes Simplex Virus 1 into Murine Epidermis: Involvement of Nectin-1 and Herpesvirus Entry Mediator as Cellular Receptors

2014 ◽  
Vol 89 (1) ◽  
pp. 262-274 ◽  
Author(s):  
Philipp Petermann ◽  
Katharina Thier ◽  
Elena Rahn ◽  
Frazer J. Rixon ◽  
Wilhelm Bloch ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Ex Vivo ◽  
Target Tissue ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
The Impact ◽  
Herpesvirus Entry Mediator ◽  
Hsv 1

ABSTRACTSkin keratinocytes represent a primary entry site for herpes simplex virus 1 (HSV-1)in vivo. The cellular proteins nectin-1 and herpesvirus entry mediator (HVEM) act as efficient receptors for both serotypes of HSV and are sufficient for disease development mediated by HSV-2 in mice. How HSV-1 enters skin and whether both nectin-1 and HVEM are involved are not known. We addressed the impact of nectin-1 during entry of HSV-1 into murine epidermis and investigated the putative contribution of HVEM. Usingex vivoinfection of murine epidermis, we showed that HSV-1 entered the basal keratinocytes of the epidermis very efficiently. In nectin-1-deficient epidermis, entry was strongly reduced. Almost no entry was observed, however, in nectin-1-deficient keratinocytes grown in culture. This observation correlated with the presence of HVEM on the keratinocyte surface in epidermis and with the lack of HVEM expression in nectin-1-deficient primary keratinocytes. Our results suggest that nectin-1 is the primary receptor in epidermis, while HVEM has a more limited role. For primary murine keratinocytes, on which nectin-1 acts as a single receptor, electron microscopy suggested that HSV-1 can enter both by direct fusion with the plasma membrane and via endocytic vesicles. Thus, we concluded that nectin-1 directs internalization into keratinocytes via alternative pathways. In summary, HSV-1 entry into epidermis was shown to strongly depend on the presence of nectin-1, but the restricted presence of HVEM can potentially replace nectin-1 as a receptor, illustrating the flexibility employed by HSV-1 to efficiently invade tissuein vivo.IMPORTANCEHerpes simplex virus (HSV) can cause a range of diseases in humans, from uncomplicated mucocutaneous lesions to life-threatening infections. The skin is one target tissue of HSV, and the question of how the virus overcomes the protective skin barrier and penetrates into the tissue to reach its receptors is still open. Previous studies analyzing entry into cells grownin vitrorevealed nectin-1 and HVEM as HSV receptors. To explore the contributions of nectin-1 and HVEM to entry into a natural target tissue, we established anex vivoinfection model. Using nectin-1- or HVEM-deficient mice, we demonstrated the distinct involvement of nectin-1 and HVEM for HSV-1 entry into epidermis and characterized the internalization pathways. Such advances in understanding the involvement of receptors in tissue are essential preconditions for unraveling HSV invasion of skin, which in turn will allow the development of antiviral reagents.

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