"Herpes Profile 2" 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.
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 IgG - This study allows us to detect IgG antibodies to HSV1 and HSV2 in blood serum. IgG antibodies against herpes simplex virus are found in 80-90% of adults, so their single definition is not clinically relevant. It is important to observe the dynamics of changes in antibody levels. Acute infection or virus reactivation has been shown to increase IgG antibody levels. IgG antibodies may have circulated throughout the body throughout life. Elevated IgG antibody levels in serum samples obtained at 7-10 day intervals indicate recurrent herpes infection.
When infected with HSV 1 and HSV 2, IgG antibodies may not be detected in the early stages of the infection.
No special preparation is required prior to testing.
Needed for the test - Venous blood.
People infected with HSV1 or HSV2 may not have noticeable levels of IgG antibodies in the early stages of infection. The increase in IgG antibody concentration begins 1-2 weeks after the initial infection, reaches a peak in 6-8 weeks, and then gradually decreases. Antibody levels may be very low or unnoticed in the period between reactivations.
Demonstration of seroconversion of IgG antibodies (negative -> positive) confirms active infection.
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