Viral infection herpes simplex

Capsaicin reduces the sensitivity of nerve cells (nocireceptors) for pain and is therefore used in medicine, in creams and sprays, against infectious diseases of the skin and mucous membranes, such as the viral infection herpes simplex and psoriasis and seems to be active in the treatment of lung and prostate cancer. 

Infections, in particular bacterial and viral (cytomegalovirus, Herpes simplex virus, Epstein-Barr virus), and also protozoal and fungal infections, are major causes of morbidity and mortality in the post-transplantation period, whatever the immunosuppressive regimen used (50-52). Based on an analysis of medical and autopsy records, infections were found to be the cause of death in 70% of transplant patients, with bacteria (50%) or fungi (29%) the most common pathogens (53). 

HSV2 (herpes simplex virus 2), which causes significant morbidity and is an important cofactor for the transmission of HIV infection was recently targeted in a mouse model by local application of siRNA mixed with lipids. The results suggested that siRNA could work as active components of microbicides to prevent viral infection or transmission [2]. 

Antiviral drugp interfere with viral reproduction by altering DNA synthesis. These drug are used in the treatment of herpes simplex infections of the eye, treatment in immunocompromised patients with cytomegalovirus (CMV) retinitis, and for the prevention of CMV retinitis in patients undergoing transplant. 

Catechins and proanthocyanidins have a documented antiviral activity. Catechins from an extract of Cocos nucifera husk fibre exhibited a strong inhibitory activity against acyclovir-resistant herpes simplex virus type 1 (HSV-l-ACVr) [62]. The use of 10 to 20ngml of ECG and EGCG has been reported to cause 50% inhibition of human immunodeficiency virus reverse transcriptase [89], while Kara and Nakayama [90] reported that a patented chewing gum containing tea catechins is claimed to prevent viral infections against influenza and to inhibit dissemination of this virus. 

Viruses may also cause latent infection of a host. In a latent infection, there is a delay between infection by the virus and the appearance of symptoms. Fever blisters (cold sores), caused by the herpes simplex virus, result from a latent viral infection the symptoms reappear sporadically as the virus emerges from latency. The latent stage in viral infection of an animal cell is generally not due to the integration of the viral genome into the genome of the animal cell, as is the case with latent infections by temperate bacteriophages. 

Despite the protective effect of NO against various viral infections, workers in several studies have shown a harmful role of NO in many systems. NO seems to play a part in the development of pneumonia caused by influenza virus [128], in the pathogenesis in mice of tick-borne encephalitis flavivirus infection [131], and in worsening the course of the murine myocarditis caused by coxsackievirus B3 [132]. In addition, pneumonia in mice induced by herpes simplex virus type 1 could be suppressed by the inhibitor of iNOS [133]. The issue of whether NO acts as an inhibitor of viral replication or as a harmful agent, therefore, remains unanswered. This issue is particularly evident in HIV-1 infection, since NO seems to act as a double-edged sword in the pathogenesis of HIV-1. 

Once the virus has achieved an intracellular location, it is protected from antibodies and only cell-mediated immunity is effective. Difficulties in producing effective vaccines against some viral infections, such as HIV, herpes simplex and hepatitis, have spurred the development of new strategies that use DNA rather than protein. 

Use with caution in patients with active or quiescent tuberculosis infections of the respiratory tract, or in untreated fungal, bacterial, or systemic viral infections, or ocular herpes simplex. 

Acute epithelial herpes simplex keratitis (dendritic keratitis) fungal diseases of ocular structures vaccinia, varicella and most other viral diseases of the cornea and conjunctiva ocular tuberculosis hypersensitivity after uncomplicated removal of a superficial corneal foreign body mycobacterial eye infection acute, purulent, untreated eye infections that may be masked or enhanced by the presence of steroids. 

The tubingensins A (379) and B (380) showed activity against the widespread crop pest Heliothis zea, and display in vitro anti-viral activity against herpes simplex virus type 1 with IC50 values of 8 and 9 pg/mL, respectively (346) (see Scheme 2.100). Some bis-basic ethers of carbazoles are anti-viral. When tested against Encephala myocarditis viral infection, several N-ethyl substituted bis-basic carbazoles of the general formula 490 were shown to be active (448) (Scheme 4.9). 

Aciclovir is phosphorylated preferentially by herpes simplex virus-coded thymidine kinase and following further phosphorylation aciclovir triphosphate interferes with herpes virus DNA polymerase and viral DNA replication. Aciclovir topical cream is indicated in the management of initial genital herpes and in limited non-life threatening mucocutaneous herpes simplex virus infections in immunocompromised patients. 

Foscarnet is an inorganic pyrophosphate analogue which causes selective inhibition of viral DNA polymerase and reverse transcriptase. Topical foscarnet cream has appeared to be a safe and effective treatment for aciclovir-unresponsive mucocutaneous herpes simplex virus infection in AIDS patients. 

Trifluoromethyl-2 -deoxyuridine, trifluridine (Viroptic ), is an anti-viral drug acting on TS via another mechanism. It is a mechanism-based inactivator of thy-midylate synthase (Figs. 27 and 28). Trifluridine is marketed for the topical treatment of Herpes simplex virus infection in eyes. 

Viral DNA polymerase is an important catalyst for the synthesis of viral nucleic acids. DNA polymerase inhibitors have already been encountered as antitumor agents. Ara-A (9.5, vidarabine) is a DNA polymerase inhibitor that has demonstrated activity against herpes simplex virus type I (HSV-1) infections, responsible for cold sores on... 

IgG receptors on cultured, human lymphocytes.526 Sialidase treatment of lymphocytes from sensitized subjects increased the responsiveness to viral, bacterial, and fungal antigens.527 The same treatment of human, Herpes simplex virus-infected cells was found to enhance the sensitivity of the cells to lysis mediated by antibody and complement.528... 

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