scholarly journals Calcium spirulan derived from Spirulina platensis inhibits herpes simplex virus 1 attachment to human keratinocytes and protects against herpes labialis

2016 ◽  
Vol 137 (1) ◽  
pp. 197-203.e3 ◽  
Author(s):  
Julia Mader ◽  
Antonio Gallo ◽  
Tim Schommartz ◽  
Wiebke Handke ◽  
Claus-Henning Nagel ◽  
...  
2019 ◽  
Vol 3 (1) ◽  
pp. 57
Author(s):  
Farhani Azizah ◽  
Irna Sufiawati ◽  
Mieke Hemiawati Satari

Pendahuluan: Salah satu virus yang menginfeksi rongga mulut adalah Herpes Simpleks Virus-1 (HSV-1). Virus ini menjadi patogen utama pada berbagai macam inang dan dapat menyebabkan berbagai macam penyakit orofasial. Tatalaksana infeksi HSV-1 memiliki pola terapi yang beragam bergantung pada kondisi klinis pasien. Tujuan penelitian ini adalah memperoleh data mengenai pola dan terapi penyakit mulut karena infeksi HSV-1. Metode: Data yang dikumpulkan merupakan data sekunder berasal dari logbook dan rekam medik pasien di Poliklinik Gigi dan Mulut RSUP Dr. Hasan Sadikin Bandung periode 2013-2017. Sampel penelitian ditentukan menggunakan metode purposive sampling, yaitu rekam medik pasien dengan diagnosis penyakit mulut karena infeksi HSV-1. Hasil: Pola penyakit mulut pada instalasi rawat jalan yaitu Recurrent Intraoral Herpes (RIH) sebanyak 84,91%, Herpes Associated Erythema Multiforme (HAEM) 9,43%, Herpes labialis 3,77%, dan Primary Herpetic Gingivo Stomatitis (PHGS) 1,89%. Pola penyakit mulut pada rawat inap yaitu Recurrent Intraoral Herpes (RIH) sebanyak 85,71% dan Herpes labialis sebanyak 14,29%. Pemberian terapi sangat bervariatif yaitu kombinasi asiklovir, antiseptik, multivitamin, antiinflamasi steroid, NSAID, pelembab bibir, antibiotik, antihistamin, dan antifungal. Simpulan: Penyakit mulut karena infeksi HSV-1 yang paling sering ditemukan baik pada instalasi rawat jalan maupun rawat inap adalah recurrent intraoral herpes. Pemberian terapi yang paling sering digunakan pada instalasi rawat jalan yaitu kombinasi obat antiinflamasi steroid dan multivitamin, sedangkan pada instalasi rawat inap yaitu multivitamin dan kombinasi asiklovir, antiseptik, dan multivitamin.Kata kunci: Pola penyakit mulut, pola terapi, infeksi Herpes Simpleks Virus-1 ABSTRACTIntroduction: One of the viruses that infect the oral cavity is Herpes Simplex Virus-1 (HSV-1). This virus becomes the primary pathogen in various types of hosts and can cause various kinds of orofacial diseases. Management of HSV-1 infection has a diverse pattern of therapy depending on the clinical condition of the patient. The purpose of this study was to obtain data on the patterns and treatment of oral diseases due to HSV-1 infection. Methods: Data collected was secondary data from the logbook and medical records of patients at the Dental Polyclinic of Dr Hasan Sadikin Hospital Bandung in 2013-2017. The study sample was determined using a purposive sampling method, namely medical records of patients with a diagnosis of oral disease due to HSV-1 infection. Results: The pattern of oral disease in outpatient installations, namely Recurrent Intraoral Herpes (RIH) 84.91%, Associated Erythema Multiforme (HAEM) Herpes 9.43%, Herpes labialis 3.77%, and Primary Herpetic Gingivo Stomatitis (PHGS) 1.89%. The pattern of oral disease in inpatient installations, namely Recurrent Intraoral Herpes (RIH) as much as 85.71% and Herpes labialis 14.29%. Given therapy was very varied, namely a combination of acyclovir, antiseptic, multivitamin, anti-inflammatory steroid, NSAIDs, lip moisturisers, antibiotics, antihistamines, and antifungal. Conclusion: Oral disease due to HSV-1 infection that is most often found both in outpatient and inpatient installations is recurrent intraoral herpes. The most commonly used therapy in outpatient installations is a combination of steroid anti-inflammatory drugs and multivitamins, while in inpatient installations are multivitamins and a combination of acyclovir, antiseptic, and multivitamins.Keywords: Oral disease patterns, therapy patterns, Herpes Simplex Virus-1 infection


2020 ◽  
Author(s):  
Nydia De La Cruz ◽  
Dagmar Knebel-Mörsdorf

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.


Author(s):  
Sergio Delmonte ◽  
Francesca Sidoti ◽  
Simone Ribero ◽  
Ivano Dal Conte ◽  
Antonio Curtoni ◽  
...  

Author(s):  
Z. Hong Zhou ◽  
Jing He ◽  
Joanita Jakana ◽  
J. D. Tatman ◽  
Frazer J. Rixon ◽  
...  

Herpes simplex virus-1 (HSV-1) is a ubiquitous virus which is implicated in diseases ranging from self-curing cold sores to life-threatening infections. The 2500 Å diameter herpes virion is composed of a glycoprotein spike containing, lipid envelope, enclosing a protein layer (the tegument) in which is embedded the capsid (which contains the dsDNA genome). The B-, and A- and C-capsids, representing different morphogenetic stages in HSV-1 infected cells, are composed of 7, and 5 structural proteins respectively. The three capsid types are organized in similar T=16 icosahedral shells with 12 pentons, 150 hexons, and 320 connecting triplexes. Our previous 3D structure study at 26 Å revealed domain features of all these structural components and suggested probable locations for the outer shell proteins, VP5, VP26, VP19c and VP23. VP5 makes up most of both pentons and hexons. VP26 appeared to bind to the VP5 subunit in hexon but not to that in penton.


2001 ◽  
Vol 74 (1) ◽  
pp. 108 ◽  
Author(s):  
Diane E. Goade ◽  
Robert A. Nofchissey ◽  
Donna F. Kusewitt ◽  
Brian Hjelle ◽  
John Kreisel ◽  
...  

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