[HTLV-I is an abbreviation for the human T-cell lymphotropic virus type 1, also called the Adult T-cell lymphoma virus type 1, a virus that has been seriously implicated in several kinds of diseases including HTLV-I-associated myelopathy, Strongyloides stercoralis hyper-infection, and a virus cancer link for leukemia (see adult T-cell leukemia/lymphoma). Between one in twenty and one in twenty-five infected persons are thought to develop cancer as a result of the virus.

HTLV was discovered in 1977 in Japan. The virus was first isolated by Drs. Bernard Poiesz and Francis Ruscetti and their co-workers in the laboratory of Robert C. Gallo at the NCI.[1] It was the first identified human retrovirus.

Infection with HTLV-I, like infection with other retroviruses, probably occurs for life and can be inferred when antibody against HTLV-1 is detected in the serum.

Prevalence
HTLV-I infection in the United States appears to be about half as prevalent as HIV infection among IV drug users and about one-tenth as prevalent in the population at large. Although little serologic data exist, prevalence of infection is thought to be highest among blacks living in the Southeast. A prevalence rate of 30% has been found among black intravenous drug abusers in New Jersey, and a rate of 49% has been found in a similar group in New Orleans.[2] It is possible that prevalence of infection is increasing in this risk group.

HTLV-I infection in Australia is very high among the Indigenous peoples of central and northern Australia, with a prevalence rate of 10-30%. It is also high among the Inuit people of Northern Canada.[1]

Studies of HTLV-I antibody indicate that the virus is endemic in southern Japan, in north eastern Iran [3], in Peru, in the Pacific coast of Colombia and Ecuador, in the Caribbean, and in Africa.

Transmission
Transmission of HTLV-I is believed to occur from mother to child via breastfeeding; by sexual contact; and through exposure to contaminated blood, either through blood transfusion or sharing of contaminated needles. The importance of the various routes of transmission is believed to vary geographically.

In Japan, the geographic clustering of infection and the rarity of unprotected sexual contact suggest that the virus is more dependent on mother-to-child transmission]
In the Caribbean, the geographic distribution of the virus is more uniform, and it is more common among those with many sexual partners, indicating that sexual transmission is more common]
Opportunistic infections
Individuals infected with HTLV-1 are at risk for opportunistic infections, diseases not caused by the virus itself, but by alterations in the host's immune functions.


Mechanism
HTLV-1, unlike the distantly related retrovirus HIV, has an immunostimulating effect, which, however, turns out to be immunosuppressive. The virus activates a subset of T-helper cells called Th1 cells. The result is a proliferation of Th1 cells and overproduction of Th1 related cytokines (mainly IFN-gamma and TNF-alpha). Feedback mechanisms of these cytokines cause a suppression of the Th2 lymphocytes and a reduction of Th2 cytokine production (maily IL-4, IL-5, IL-10 and IL-13). The end result is a reduction in the ability of the infected host to mount an adequate immune response to invading organisms that require a predominantly Th2 dependant response (these include parasitic infections and production of mucosal and humoral antibodies).


[Examples
In the central Australian Aboriginal population, HTLV-1 is thought to be related to their extremely high rate of death from sepsis.

It is particularly associated with bronchiectasis, a chronic lung condition predisposing to recurrent pneumonia.

It is also associated with chronic infected dermatitis, often superinfected with Staphylococcus aureus and a severe form of Strongyloides stercoralis infection called hyper-infection which may lead to death from polymicrobial sepsis.

HTLV-1 is also associated with adult T cell leukemia/lymphoma, and has been quite well studied in Japan. The time between infection and onset of cancer also varies geographically. It is believed to be about sixty years in Japan, and less than forty years in the Caribbean. The cancer is thought to be due to the pro-oncogenic effect of viral DNA incorporated into host lymphocyte DNA, and chronic stimulation of the lymphocytes at the cytokine level may play a role in development of malignancy. The malignancy ranges from a very indolent and slowly progressive lymphoma to a very aggressive and nearly uniformaly lethal proliferative lymphoma. Treatment varies depending on the type of disease and varies from careful observation to aggressive chemotherapy and antiretroviral agents.

HTLV-1 is also associated with a progressive demyelinating upper motor neurone disease known as HAM/TSP for HTLV-1 associated myelopathy/Tropical Spastic Paparparesis characterized by sensory and motor defecits, particularly of the lower extremeties, incontinence and impotence. [6] Less that 2% of infected individuals develop HAM/TSP, but this will vary dramatically from one geographic location to another.


[ HTLV-II
A virus closely related to HTLV-I, HTLV-II shares approximately 70% genomic homology (structural similarity) with HTLV-I.

It is found predominantly in IV drug users and Native Americans, as well as Caribbean and South American Indian groups.

HTLV-II has not been clearly linked to any disease, but has been associated with several cases of myelopathy/tropical spastic paraparesis (HAM/TSP)- like neurological disease.


HTLV-III and HTLV-IV
The terms "HTLV-III" and "HTLV-IV" have been used to describe recently characterized viruses.[7][8]

These viruses were discovered in 2005 in rural Cameroon, and were apparently transmitted from monkeys to hunters of monkeys through bites and scratches. HTLV-III is similar to STLV-III (Simian T-lymphotropic virus 3), but HTLV-IV does not resemble any known virus. It is not yet known how much further transmission has occurred among humans, or whether the viruses can cause disease.

The use of these names can cause some confusion, because the name HTLV-III was the former name of HIV in early AIDS literature, but has since fallen out of use.[9]. Also, the name HTLV-IV has been used to describe HIV-2.[10][/LEFT]

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HIV P24 Ag

The human immunodeficiency virus (HIV 1 and 2) is a retrovirus and is the causative agent of AIDS.

HIV is transmitted by the parenteral route, mainly through sexual contact, mother-to-infant transmission and, less commonly, by blood or intravenous drug use.

Infection with HIV leads initially to a mild glandular fever-like illness 2-3 weeks after infection. In addition to the clinical symptoms, the CD4 cell count is lowered for a time. Most HIV infected individuals recover from this initial infection within 2-3 weeks, seroconvert and then remain asymptomatic for 5-10 years. However, during this period, individuals actually appear to undergo a persistent chronic infection which causes a gradual decline in CD4 cell numbers. When these numbers fall below a certain level the individual becomes susceptible to a number of infections and the symptoms marking the start of full-blown AIDS appear.

Detection of HIV:
An HIV infection diagnosed through the detection of virus, rather than indirectly through the detection of antibodies, because of its higher cost, should only be undertaken if indicated.
Virus isolation in cell cultures is reserved for special cases requires the use of a high-security laboratory
The p24 test identifies actual HIV viral particles in blood (p24 is a protein found in HIV). However, the p24 test is generally only positive from about one week to 3 - 5 weeks after infection with HIV. The p24 protein cannot be detected until about a week after infection with HIV because it generally takes that long for the virus to become established and multiply to sufficient numbers that they can be detected. The p24 proteins then become undetectable again after sufficient antibodies to HIV have been produced because they bind to the p24 protein and eliminate it from the blood.

Once antibodies are produced, the p24 test will register negative even in people who are infected with HIV. At that point, the regular HIV antibody test will then be positive. Later in the course of HIV, p24 protein levels again become detectable.

Problem: The "diagnostic window"
One important problem of HIV antibody testing is the so-called "diagnostic window". This is the time period between the HIV infection until detectable levels of antibodies are present. The switch from antibody-negative to antibody-positive is called "seroconversion". The screening tests currently used are able to recognize an HIV infection six weeks after primary infection in about 80 % and after the 12th week in almost 100 % of cases; only in very rare cases an infection is recognized only after three or even six months. 4th generation screening assays attempt to shorten the duration of the "diagnostic window" by detecting HIV antibodies and HIV p24 antigen simultaneously (combo test).
Conclusion:
1. HIV viral load (by PCR): can be detected after 10 days from infection.
2. HIV P24 Ag: can be detected after 20 days from infection up to 50 days.
3. HIV Abs: can be detected after 30 days from infection and persist for long time.
4. HIV western blot technique: used as a confirmatory test for HIV abs positive cases

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