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  • fuckedgaijin ‹ General ‹ Gaijin Ghetto

HTLV-I - In areas of Japan up to 30% are you FGs aware?

Groovin' in the Gaijin Gulag
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Have you been told about HTLV-I before? -Especially the risk in JP?

 
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HTLV-I - In areas of Japan up to 30% are you FGs aware?

Postby japslapper » Sun Oct 26, 2003 6:58 pm

Routes of transmission
Vertical via maternal HTLV-I infected T cells in breast milk
Sexual transmission - male to female, male to male and rarely female to male.
Transfusion related cases via receipt of blood with infected T cells.
Injection Drug Use as a consequence of sharing contaminated equipment


Surveys have noted that this virus is endemic in southern Japan, the Caribbean (3-6%), Central and South America and areas of Africa. In areas of Japan up to 30% of the population are seropositive. 1% of the Japanese population are carriers for HTLV-I but 98% of infected individuals remain asymptomatic. The lifetime risk of adult-T-cell leukaemia in a carrier is 2-4% whilst the lifetime risk of myelopathy is 0.25%


http://www.link.med.ed.ac.uk/RIDU/Htlv.htm

http://www.thebody.com/sowadsky/answers/

http://www.bcm.tmc.edu/neurol/challeng/pat58/summary.html

I have an MS in biology and had never realised the risks before (though its very very rare in the UK) 8O

We all know that Japan has a low HIV rate(alegedly :? ) so I notice some trolls on this site brag about their 40+ Japan "conquests" - I wonder if they are lax with precautions :idea: :?:

Any FGs from down South(Kyshu/Okinawa) with any observations :?:

Note FGs that in schools safesex education is dodgy and the J-medics (in my experience) do not question statistics from "Head Office" :evil: - I will ask my local Doc if he knows anything of HTLV-I........ :cry:

Scarry 8O
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Re: HTLV-I - In areas of Japan up to 30% are you FGs aware?

Postby Taro Toporific » Sun Oct 26, 2003 8:31 pm

japslapper wrote:
Routes of transmission
... HTLV-I infected T cells in breast milk .....
.....so I notice some trolls on this site brag about their 40+ Japan "conquests" - I wonder if they are lax with precautions :idea: :?:


Damn. I thought this tittie looked odd.
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Postby japslapper » Mon Oct 27, 2003 12:47 am

Damn. I thought this tittie looked odd.


Nice picture Taro :lol: .....try and find a tittie with kitty chan/pooh san next time - that would convincingly be Japanese!

Seriously FGs - if you look through SciAM or and other sci. journals this HTLV-I virus could be worse than the current HIV problem.

FGs "protect your self" :wink:



.....Japan is really pissing me off at the mo - I cannot stand the dishonesty/dont lose face bit - this has lethal consequences for other people and thus is selfish :evil: :evil:
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Postby American Oyaji » Mon Oct 27, 2003 1:50 am

what is HTLV?
I will not abide ignorant intolerance just for the sake of getting along.
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Postby japslapper » Mon Oct 27, 2003 2:09 am

Whats is HTLV? :?: :?: :?:


Exogenous Human oncoviruses. Single family the human T-lymphotropic viruses. They are unrelated to human endogenous viruses. Similar in organization to bovine leukemia virus and simian T-lymphotropic virus.

Human T Leukemia Viruses

Unlike the situation with rodents and avian sources it has been very difficult to isolate true human retroviruses. Within the last ten years, this has become possible because of changes in growing human cells, mostly as the result of the discovery of growth factors, and the development of sensitive assays for the reverse transcriptase.

When T-cells are treated with a mitogen, such as PHA you get some limited growth. The medium from such cells contains among other factors a T-cell growth factor, now known as IL-2. The mitogen also stimulates the production of receptor sites for the growth factor, the IL-2 receptor.

IL-2 is a protein of 15,000 mol.wt with little host specificity. It activates mature cells of the T-cell lineage provided they have receptors. Normal T cells are not activated, however malignant T-cells or mitogen treated T-cells which develop receptors are activated.

Monoclonal antibody to surface receptors has been produced, known as Tac antigen. This monoclonal recognizes a component of the T-cell receptor. It was found that antibodies from leukemia patients reacted against the retrovirus cultured in a cell line from a patient with ATL.

This virus was called HTLV-1.

To identify HTLV infected cells, harvest lymphocytes from Ficoll gradient, treat 48-72 hours with PHA, and grow in complete medium with 20% serum and 10% IL-2. Virus detected by reverse transcriptase activity or by E.M.

HTLV-1 first discovered in two patients with ATL, same as high incidence Japanese leukemia.

ATL

In 1977 recognized in Japan that adult T-cell leukemia ( ATL) was a unique disease characterized by an unusual geographical distribution , not unlike that seen in the case of Burkitt's lymphoma. ATL was found predominantly in the Southern Japanese Island of Kyushu, and the Northern Island of Hokkaido. Very little found in central Japan. Such geographic patterns suggest that genetic, environmental or infectious agent interacting to produce the disease.

Over the next few years the relationship between ATL and HTLV-1 was strengthened.

There was a direct relationship between the clusters of ATL seen in Japan and HTLV-1.
Also virus discovered in other pockets in the Caribbean, in Taiwan and in Papua New Guinea.. When virus was isolated from these diverse regions, some 96-99% of the nucleotide sequence was identical. Shown that every ATL patient was infected with HTLV-1. Tumors taken from such patients all contained some HTLV-1 material. When HTLV-1 grown with normal T-cells virus integrated into chromosome and immortalizes cells. Virus shown to be related to BLV and STLV-1. Possible to fulfill Koch's postulates with BLV and STLV-1.

Major mystery is how virus maintains a 20-40 year latent period, and promoted T-cell leukemia in 0.1% of infected individuals. Also why the peculiar geographic distribution.

Adult T-cell leukemias are TAC+ .All malignancies associated with HTLV are also TAC+. The number of TAC receptor sites is much elevated following HTLV infection compared to mitogen stimulation.

This is good example how modern biotechnology allows for the analysis and characterization, identification of a virus.

Virus characterized by immunological cross reactivities of the viral proteins, sequence homology by molecular hybridization, cleavage pattern by restriction enzymes and finally nucleotide sequence analysis.

All HTLV have common features

Isolated from mature T-cells.
Mainly infect CD4+ cells
Immunological cross reactivity between internal core proteins
Reverse transcriptase of similar size and biochemical features.
Three major groups of HTLV have been described to date:

HTLV-1, associated with human adult T-cell leukemia (ATL) This is an infectious disease, and is endemic in S.Japan, and the Caribbean,
HTLV-2 originally isolated from patients with T-cell hairy leukemia (Mo-1).
HTLV-3, Isolated from patients with AIDS, and now called HIV.
All these viruses share the same features. However HTLV -III only distantly related to I and II. HTLV-1 and II differ in envelope protein.

The size varies from 90-140 nm,isolated from mature T cells,

selective tropism for OKT4+ T cells, Immunologically cross reactive core protein, and reverse transcriptase of similar size and biochemical properties.

Each virus contains two copies of the viral RNA hydrogen bonded to each other by means of palindromic sequences some 40 nucleotides long about 60-80 nucleotides from their 5' ends.

HTLV genome

The organization of the HTLV genome is similar to that of other retroviruses. The provirus sequence is 9032 nucleotides long, flanked by a terminal repeat of about 750 bp. and has two long LTR sequences. The extra long LTR is due to a larger than usual R and U5 region. The genome consists of the usual gag-pol-env genes, but also contains a large ORF (tax) between the env and the LTR, which in different reading frames codes for two proteins, tax and rex.

The tax protein is involved in transforming activity of the virus, and in the phenomenon of trans-activator of transcriptional regulation. The Tax product upregulates transcription of all the viral genes in the integrated HTLV proviral DNA and initiates the leukemogenec process. This is defined as a greatly increased rate of transcription directed by the viral LTR in infected as compared to uninfected cells.

A second HTLV regulatory gene , rex, regulates the splicing of RNA transcripts by promoting the production and transport to the cytoplasm of unspliced viral RNA and the incompletely spliced gag/pol and env mRNAs, so allowing the production of new virions. Rex has a negative effect on its own production and that of tax, Rex may be responsible for latency. The tax gene not only acts as trancriptional enhancer of viral genes but also cellular genes, particulary IL-2 receptor, thus leading to autocrine stimulation of T-lymphocytes. Also enhances production of NF-kB, and thus may serve as cofactor in AIDS by inducing replication of integrated HIV.
Cellular Pathology

T4 lymphocytes are the specific targets of all HTLVs. Tumors induced after HTLV 1 infection occur after a long latent period, and with a low incidence. Tumors of HTLV 1 are monoclonal with respect to integration site. They can also transform cells in culture, and give rise to indefinite growth of T-cells. There are reports of transformation of B-lymphocytes, fibroblasts and endothelial cells.

One of the major differences between infected and non-infected T-cells is the appearance of IL-2 receptors. They show partial or complete independence of IL-2, express high levels of receptors and HLA-DR determinants, as well as morphological differences. The immunological functions of the T cells are impaired, and the individual becomes susceptible to opportunistic infections.

Epidemiology

Sera of patients with a variety of malignancies and a number of control sera were screened for antibodies to HTLV-1 proteins. The methods employed included (a) Solid phase immunoassays using disrupted viral particles. (b) radioimmune precipitation assays using pure HTLV-1 p24,p19,and p15 and (c) indirect immunofluoresence assy against virus infected cells. Results.

Sera with patients with ATL are almost always positive for antibodies to HTLV-I. Normal individuals and patients with non T cell leukemias are negative. In Japan find about 15-16% population(30% in Okinawa) are carriers in endemic regions. Discuss the epidemiology of the disease

Disease appears to be spread predominantly from mother to offspring in utero by passage of infected lymphocytes across the placenta or in mild form during nursing thus acquired early in life. Disease possible sexually transmitted by presence of infected lymphocytes in semen.. Studies have shown that wives of HTLV-1 positive men are more likely to be HTLV positive than wives of HTLV negative individuals. 2 antibody prevalence continues to increase in woman after the age of 40 while remaining constant in men after that age, suggesting predominantly male to female transmission, and detection of HTLV positive lymphocytes in semen from seropositive men.

Other means of spread include through blood, needles and within families by close contact. The calculated latency period for the onset of the disease is between 10 and 30 years. Of those positive, the possibility of the disease is low, about 0.1%.Very high incidence among homosexual men. In Trinidad 15% male homosexuals were positive for HTLV-1 antibodies as opposed to 2.4% in the general population.

The incidence of the disease in on the increase in the U.S. Spread very much like AIDS. The average survival rate of the ATL patient is 11 months. In all cases HTLV-1 appears to spread through infected cells and not as a free virus.

Transmission in very inefficient, requiring multiple exposures through breast feeding or sexual intercourse

Using molecular probes,i.e. Southern blots, find very similar results. Fresh cells from all patients with ATL contain one or few copies of HTLV. In some cases find only partial virus, env and LTR. The site of integration of the HTLV-I provirus in different patients was different. No two patients had the same flanking sequences around the integrated provirus. Thus integration is monoclonal or oligoclonal. Probable that an HLTV infection preceded the integration and that there was some selection for fast growing cell.

If mix normal T lymphocytes with infected cells can infect and transform these T lymphocytes in culture.

Infected replicating cells became apparent after 3 to 6 weeks in culture. Did not need TCGF.

HTLV appears to affect the function of T-cells. Such T-cells appear to have increased helper function and may be non-specifically activated to stimulate B-cells. Also loss of cytotxic T-cell function. These observations suggested that HTLV infection might induce immune deficiency and cause polyclonal B-cell activation.




http://www.bio.indiana.edu/courses/M430-Taylor-virology/htlv.html


:idea: : 8O 8O 8O 8O :?: :idea:
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Postby japslapper » Mon Oct 27, 2003 2:41 am

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Postby AssKissinger » Mon Oct 27, 2003 6:43 am

The incidence of the disease in on the increase in the U.S. Spread very much like AIDS. The average survival rate of the ATL patient is 11 months. In all cases HTLV-1 appears to spread through infected cells and not as a free virus.

Damn. Sounds scary as Hell. JS, you have an MS biology? At the risk of sounding like a nincompoop most of your links are over my head. Could you explain exactly what this is in simpler terms? Thank-you.
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Postby Caustic Saint » Mon Oct 27, 2003 8:03 am

I'm not a doctor, nor do I play one on TV, but this sounds like a second cousin to HIV - kind of like a communicable form of leukemia.

Ever get the feeling that maybe the world is trying to shrug us off, like a bad case of fleas?
More caustic. Less saint. :twisted:
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Postby Robato » Mon Oct 27, 2003 9:05 am

why is HIV considered HTLV-III? Was HTLV-I discovered first? If it was, how come nobody has ever heard of it?
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Itty-bitties

Postby Taro Toporific » Mon Oct 27, 2003 9:40 am

japslapper wrote:Nice picture Taro :lol: .....try and find a tittie with kitty chan/pooh san next time ....


You want Kitty Titties? Ok :arrow: Image

Routes of transmission
Vertical via maternal HTLV-I infected T cells in breast milk
Sexual transmission - male to female, male to male and rarely female to male.
Transfusion related cases via receipt of blood with infected T cells.
Injection Drug Use as a consequence of sharing contaminated equipment

...I will ask my local Doc if he knows anything of HTLV-I........


If you have a Masters in Microbio you know more than 99.9999999% of the Japanese doctors. Use of broad-spectrum antibiotics without an culture-&-sensitivity test is the norm in Japanaese malpractice of medicine.

What I was teasing you about the Doraemon tit was that routes of transmission HTLV-I such breast feeding aren't a big concern for the average FG male.Image
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Postby japslapper » Wed Oct 29, 2003 7:18 pm

Damn. Sounds scary as Hell. JS, you have an MS biology? At the risk of sounding like a nincompoop most of your links are over my head. Could you explain exactly what this is in simpler terms? Thank-you.


AssKinger - bascically this bug is a bit like HIV in its biology - its sexually transmitted, effects a similar part of the immune system (CD4 cells - which are part of the bodies immune defence system) though it is not as virulent as HIV - in that I mean you need to bonk quiet a bit more to raise the risk substantially. This disease, if you catch gives you a 2%chance of contracting leukemia(fatal) or a few other symptoms - usually mental in manifestation....... however take note this disease is not as well researched or talked about as HIV - mainly becaues it is not so well spread and its main location is S.Jp and offcourse you will have the J-government not wanting to lose (international) standing by admiting this problem - HIV is mentioned because it was started by smelly gaijin :roll:



If you have a Masters in Microbio you know more than 99.9999999% of the Japanese doctors. Use of broad-spectrum antibiotics without an culture-&-sensitivity test is the norm in Japanaese malpractice of medicine.


Penicillan allergy wots that? :roll: :evil:



why is HIV considered HTLV-III? Was HTLV-I discovered first? If it was, how come nobody has ever heard of it?


HIV and HTLV are a collection of auto immune diseases which I suspect have been in human populations for a long time - they could have the same evoluntionary route . The main point why HTLV is not so mentioned is that its discovery is quite recent, it is not so lethel, short term as HIV and ofcoures that it is centred on Japan :roll:

Moral of the story - don`t shag Japanese from Okinawa, Hokaido. Thoses FGs going bareback in Nagoya have the least risk on this front - apart from the demands of an expensive wedding :lol:
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Postby American Oyaji » Wed Oct 29, 2003 11:21 pm

No shagging until I get remarried.
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Postby japslapper » Thu Oct 30, 2003 1:51 am

No shagging until I get remarried.


In "Mad Yank" English, shagging means dancing and in Brit English it means horizontal jogging - which one are you on about?
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Postby Robato » Thu Oct 30, 2003 5:12 am

japslapper wrote:
No shagging until I get remarried.


In "Mad Yank" English, shagging means dancing and in Brit English it means horizontal jogging - which one are you on about?


In American English it means "brits say this for fuck" :lol:

I also hear brits call cigarettes "fags"......"Hey man, get that fag out of your mouth so we can shag!!"
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