Herpes prevention

Prevention of the herpes simplex virus is essential for patients who have a history of the infection (a single incidence of herpes is enough). Herpes prevention is necessary with a peel to the papillary dermis. It is also worthwhile when a more superficial peel is usually accompanied by a severe inflammatory reaction, as is the case with resorcinol, classic AHAs and TCA-SAS. It is not necessary when using Easy TCA imder its basic protocol or Easy Phytic . General infection prevention measures should be taken, depending on the depth of the peel. For more information, see the discussion of infections in Chapter 37. 

Herpes prevention is essential before a TCA-SAS peel, as the dermis of the skin has to be destroyed for the peel to be effective, and the skin s immune defenses suffer from this destruction. ETCA is more stimulating than destructive it will not destroy the skin s immune defenses. On the contrary, repeated peels appear instead to stimulate it. No herpes prevention is necessary before using ETCA in the basic protocol (scattered pinpoint or cloudy white frosting). 

The risk of bacterial or viral complications with medium or deep peels could lead doctors to think that, in order to avoid these problems, only superficial peels should be performed and patients with active acne or herpes should not be treated at all. With a medium or deep peel, herpes prevention - as far as it goes - consists in a sandwich treatment with aciclovir, which is not well tolerated by patients with sensitive stomachs. With acne, caution limits the range of treatment choice to careftjl superficial peels (which have limited effectiveness even after repeated sessions). We are forced to put off, sometimes indefinitely, performing medium-depth peels on patients with acne or herpes that have not responded to preliminary medical treatment. 

Depending on how prone the patient is to herpes, valaci-clovir can be used to prevent it. Patients who say they have only had one outbreak of herpes, 20 years ago , can quite reasonably be treated without any herpes prevention if the peel does not go beyond the Grenz zone (Easy TCA -cloudy frosting), but they should stiU be closely monitored. Patients who say they suffer from herpes all the time and at the drop of a hat should, of course, automatically receive Herpes prevention. 

A person who has had even just one outbreak of labial herpes in their life is at serious risk of a recurrence in the days following a peel to the papillary or reticular dermis. This cannot be considered as just a potential complication. On the contrary, it should be considered as an almost certain side-effect of peels to these depths. Herpes prevention is therefore obligatory. Only Touch is a deep peel that reaches the reticular dermis, but because its use is limited to areas of 1 cm in diameter at most, the immune defenses are not damaged enough to trigger herpes, and there have been no cases of herpes described after this peel. No prevention is necessary. 

Herpes prevention is sometimes advisable with a peel to the Grenz zone, and is essential with peels to the papillary or reticular dermis (except for Only Touch see above). 

The antiviral mechanism of action of acyclovir has been reviewed (72). Acyclovir is converted to the monophosphate in herpes vims-infected cells (but only to a limited extent in uninfected cells) by viral-induced thymidine kinase. It is then further phosphorylated by host cell guanosine monophosphate (GMP) kinase to acyclovir diphosphate [66341 -17-1], which in turn is phosphorylated to the triphosphate by unidentified cellular en2ymes. Acyclovir triphosphate [66341 -18-2] inhibits HSV-1 viral DNA polymerase but not cellular DNA polymerase. As a result, acyclovir is 300 to 3000 times more toxic to herpes vimses in an HSV-infected cell than to the cell itself. Studies have shown that a once-daily dose of acyclovir is effective in prevention of recurrent HSV-2 genital herpes (1). HCMV, on the other hand, is relatively uninhibited by acyclovir. 

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]. 

These drugp possess anti-inflammatory activity and are used for inflammatory conditions, such as allergic conjunctivitis, keratitis, herpes zoster keratitis, and inflammation of the iris. Corticosteroids also may be used after injury to the cornea or after corneal transplants to prevent rejection. 

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. 

Potentially, interferon is an ideal anhviral agent in that it acts on many different vimses and is not toxic to host cells. However, the exploitation of this agent in the treatment of viral infechons has been delayed by a number of factors. For example, it has proved to be species-specific and interferons raised in animal sources offered little protechon to human cells. Human interferon is thus needed for the treatment of human infechons and the produehon and purificahon of human interferon on a large scale has proved difficult. The inserhon of human genes for interferon into E. coli has resolved the produehon problems (Chapter 24). Clinical trials have demonstrated that interferon prevents rhinovirus infeehon and has a beneficial effect in herpes, cytomegalovims and hepahtis B vims infechons. 

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. 

The most widely studied therapeutic proteins produced in plants include monoclonal antibodies for passive immunotherapy and antigens for use as oral vaccines [40]. Antibodies against dental caries, rheumatoid arthritis, cholera, E. coli diarrhea, malaria, certain cancers, Norwalk virus, HIV, rhinovirus, influenza, hepatitis B virus and herpes simplex virus have been produced in transgenic plants. However, the anti-Streptococcus mutans secretory antibody for the prevention of dental caries is the only plant-derived antibody currently in Phase II clinical trials [40]. Until recently, most antibodies were expressed in tobacco, potato, alfalfa, soybean, rice and wheat [9], It has been estimated that for every 170 tons of harvested tobacco, 100 tons represents harvested leaves. A single hectare could thus yield 50 kg of secretory IgA [3, 41]. Furthermore, it has been estimated that the cost of antibody production in plants is half that in transgenic animals and 20 times lower than in mammalian cell cul-... 

For other plant-derived antibodies, stability was shown to be similar to mammalian counterparts. For instance, a humanized anti-herpes simplex virus monoclonal antibody (IgGl) was expressed in soybean and showed stability in human semen and cervical mucus over 24 h similar to the antibody obtained from mammalian cell culture. In addition, the plant-derived and mammalian antibodies were tested in a standard neutralization assay with no apparent differences in their ability to neutralize HSV-2. As glycans may play a role in immune exclusion mechanisms in mucus, the diffusion of these monoclonal antibodies in human cerival mucus was tested. No differences were found in terms of the prevention of vaginal HSV-2 transmission in a mouse model, i.e. the plant-derived antibody provided efficient protection against a vaginal inoculum of HSV-2 [58]. This shows that glycosylation differences do not necessarily affect efficacy. 

The goals of therapy in genital herpes infection are to shorten the clinical course, prevent complications, prevent the development of latency and/or subsequent recurrences, decrease disease transmission, and eliminate established latency. 

Oral acyclovir, valacyclovir, and famciclovir are the treatments of choice for outpatients with first-episode genital herpes. Treatment does not prevent latency or alter the subsequent frequency and severity of recurrences. 

Herpes Zoster (Shingles) Zostavax is a live attenuated varicella-zoster virus (VZV) vaccine for the prevention of herpes zoster in individuals 60 years or older. It is supplied in frozen lyophilized form and reconstituted before vaccination. The vaccine boosts VZV-specific immunity and protects individuals against zosters and its complications. 

Let s conclude this discussion of life with a short consideration of viruses. Viruses cause all sorts of problems for living organisms. The problems are the consequence of their ability to infect, and ultimately kiU, many types of cells— bacterial, animal, and plant—though each virus is quite specific in terms of the type of cell that it infects. There are many types of viruses. In people, they cause measles, mumps, influenza, AIDS, polio, potentially fatal diarrhea in infants and very young children, herpes, chicken pox, shingles, the common cold, and many other diseases, that may be fatal, serious, and not so serious. In other animals, viruses also cause any number of diseases, as they do in plants. Much effort has been, and continues to be, devoted to the prevention, diagnosis, and treatment of viral diseases. 

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