Sexually transmitted diseases - Herpes
Genital herpes, also commonly called "herpes," is a sexually transmitted disease (STD) caused by the herpes simplex viruses. There are eight members of the herpes virus family that are known to cause human disease which include the varicella-zoster virus (VZV, or HHV-3) that causes chickenpox and shingles, Epstein-Barr virus (EBV, or HHV-4), cytomegalovirus (CMV, or HHV-5), human B cell lymphatic virus (HHV-6), roseola poorly characterized virus (HHV-7), and the Kaposi's sarcoma-associated herpes virus (KSHV, or HHV-8) and the commonest, herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2) which are known to cause painful, watery blisters in the skin or mucous membranes (such as the mouth or lips) or on the genitals and the rectum.
It is also known as Cold Sore, Night Fever, or Fever Blister to some doctors and is contagious, most particularly during an outbreak, and presently has no known cure yet although there are already researched medications and temporary treatments available for the prevention of the disease to get worsen.
Symptoms and complications
A person infected with the infection or the disease may manifest some blistering in the skin or the mucous membranes (such as the mouth or lips), the genitals or the rectum. They sever, often leaving tender ulcers (sores) that usually take two to four weeks to heal if it’s the first time it occurred. Normally, another occurrence can materialize weeks or months, but it almost always shorter than the first occurrence and is less severe. The number of occurrence would likely to decrease over a period of years, the infection can settle in the body indefinitely though.
Research shows that an infected person can still be contagious (actively shedding virus) up to 7-10 days the first blister healed and during this time, the asymptomatic person should still be extremely cautious.
Transmission
The virus passes through the nerve fibers to the spot of the original infection and when it reaches back the skin, redness and blisters would occur. The outbreak is critically related to the operation of the immune system and generally attacks women who have suppressed immune systems, either because of stress, infection, or medications, and usually is manifested longer and more frequently. The incubation period of the virus lasts 3 to 7 days however there will still be no symptoms and possibly can be transmitted to someone else. It’s most contagious from the time it’s itching until the ulcer reaches healing stage. Research in the 1980s indicated that the virus can be shed from the skin even if there’re no symptoms and it is estimated that among 50% and 80% of new HSV-2 cases arise from asymptomatic viral shedding.
Treatment
There is still no known cure for herpes but there are temporary medications for the outbreaks. Among them are oral medications, such as aciclovir (Zovirax), famciclovir (Famvir), or valacyclovir (Valtrex) as well as ointments that can be used to help alleviate the pain associated with the outbreak even shorten the extent of the eruption.
Docosanol (Abreva) can also be used as treatment and may be effective. It works by stopping the virus from fusing to cell membranes; hence it bars entry for the virus into the cell and may keep an eruption limited to a smaller area than would be observable.
Other antiviral drug such as Tromantadine can be very effective against herpes as well as non-prescription analgesics so as to reduce pain and fever during initial outbreaks. Recent studies recommends the use of other natural compounds such as Carrageenans, linear sulphated polysaccharides that can be extracted from red seaweeds, Resveratrol, a compound in red wine and Lactoferrin, a component of whey protein . They are found to have antiviral effects in HSV-infected cells, prevent HSV reproduction in vitro by restraining a protein needed by the virus to reproduce and have a synergistic effect with aciclovir against HSV in vitro.
The immune system is however is able to demolish active herpes virus particles but the virus can conveniently hide from the immune system in an inactive (or latent) state. Current research recommends that this ability to hide is achieved via modification to cellular enzyme histone deacetylases (HDACs), namely HDAC1 and HDAC2.
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