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"Herpes Profile 1" includes a study of the following parameters:
Herpes simplex virus (HSV) It is an ancient and ubiquitous virus that causes acute and recurrent infections in humans. Transmission occurs through close contact with infected people. The virus enters the mucous membranes (eyes, mouth and genitals) and multiplies locally. The clinical course of the infection is variable and the symptoms can sometimes be minimal and unnoticed. Mainly develops rash, skin damage, genital tract damage and herpes of the newborn. In a small percentage of those infected, the virus can enter the lymph node of a sensitive nerve root and cause recurrent (recurrent) infections. Very often, the infection is asymptomatic and the virus remains latent (dormant). Its reactivation usually occurs under the influence of external factors such as immunosuppression, stress or other infection.
Getting a positive result indicates an active infection.
Reactivation of the virus may or may not result in a marked increase in IgM antibody levels.
There are two main types of herpes virus: HSV1 and HSV2.
The first type of herpes simplex virus (HSV-1) causes herpes first, which mainly affects the skin, lips, mucous membranes of the mouth, conjunctiva, upper extremities, causing meningoencephalitis, neonatal herpes, and congenital ophthalmopathy.
Primary HSV1 infections are predominantly acquired in childhood; After an oropharyngeal infection, the virus colonizes the trigeminal ganglion, where it remains dormant. The most important clinical manifestation in children is gingivostomatitis, while in older age it is characterized by upper respiratory tract infections and infectious mononucleosis-like syndrome.
The second type of herpes simplex virus (HSV II) causes herpes for the first time by infecting the skin and genitals, buttocks, lower extremities. Causes meningoencephalitis, neonatal herpes, congenital herpes, myelitis and encephalitis. The prevalence of HSV1 infections in the general population is 70-80%, while the prevalence of HSV2 is approximately 17-25%.
Genital herpes can be caused by both HSV1 (15% of cases) and HSV2 (85% of cases). It is a sexually transmitted disease, characterized by lesions in the genital area in the form of small vesicles filled with serous contents, which are easily disintegrated and painful ulcers appear in their place, the injury may be accompanied by pain and burning sensation when urinating. Other symptoms may include itching and lymphadenopathy. Often the first lesions are accompanied by systemic symptoms such as fever, headache, photophobia, myalgia, and general weakness.
Although HSV1 and HSV2 are transmitted in different ways and affect different areas of the body, there is often a cross between the epidemiology of these two viruses and the clinical manifestations of the infections caused by them.
Differentiation between HSV1 and HSV2 infections is useful in patients with subclinical or unnoticed infections. The main situations in which it is particularly important to differentiate between HSV1 and HSV2 are:
HSV infections are usually diagnosed based on clinical manifestations and laboratory tests such as viral DNA detection, viral cultures, and serological tests.
Evaluation of serological markers (IgM, IgG) is an indirect method of diagnosing infection - it allows us to assess the body's immune response to a pathogen in the body.
Determination of IgM - This study allows us to detect IgM antibodies to HSV1 and HSV2 in blood serum. Detection of IgM antibodies is useful in confirming active infection. This is the earliest blood test that can be used to detect herpes.
Anti-HSV antibodies appear at 2-3 weeks of acute infection, with peak antibody levels observed 4-6 weeks after the development of the clinical picture of the disease. Elevated IgM antibody levels in serum samples taken at 7-10 day intervals indicate first infection. Re-infection in individuals with pre-existing IgM antibodies does not cause a significant change in their levels, even with a pronounced clinical picture. In the case of HSV1, the mean time for seroconversion (disappearance of IgM) is 3,5 weeks.
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