[I am scared by the rash under the lips, a whole patch of redness DSC specialist said is eczema with no biopsy done. You can see tiny dead skins and at times strings of dead skins. You feel the tightness when it got painful, usually at the side of the lips. It started around the time when Singapore is recently very air polluted, but might be due also to wheat allergy, or also with the exposure to intense sunshine… due to my insisted walks in the garden. I am scared because I don’t know what it is. ARS rash? Or late stage HIV rash? Will it ever recover? The specialist said it isn’t contagious… I don’t really trust a good kiss on that one diagnosis~]

HIV

Singapore specialists will usually dismiss non-official issues about STDs and many patients would hence need to be updated on HIV. Yes, seronegative infected HIV patients were all around…

Seronegative HIV Infection

A case report serves as a reminder that such infection does occur, sometimes with fatal consequences.

Seronegative HIV infection has been described previously but is quite unusual. In this brief report from Portugal, investigators described the phylogenetic analysis of a virulent HIV strain that resulted in a patient’s rapid progression to AIDS and death.The patient was a previously healthy 20-year-old heterosexual man who presented with fatigue and weight loss. Testing for infectious diseases, including serologic assays to detect antibodies to HIV-1 and HIV-2, provided no answers. Within 3 months, the patient developed oropharyngeal candidiasis, and his CD4 count dropped to 232 cells/mm3. HIV serology continued to be negative, even when his CD4 count dropped further, to 52 cells/mm3. Serum p24 antigen levels and plasma viral load were consistent with HIV infection. Within 6 months of his original presentation, he died of AIDS.

Immediately before symptom onset, the patient had a 3-month relationship with a woman who was a sex worker and injection-drug user. She, too, experienced an aggressive course of disease, presenting with a CD4 count of 40 cells/mm3 and succumbing to AIDS within 21 months. In her case, serologic testing did reveal HIV infection.

Phylogenetic testing confirmed that both patients were infected with a B/G recombinant variant that resembled a strain previously detected among injection-drug users in Spain and Portugal. Based on the presence of a heterogeneous virus population in the woman and a single virus population (all CCR5-tropic) in the man, researchers determined that transmission occurred from the woman to the man.

Comment: This case report serves as a reminder that when patients with symptoms of HIV infection have negative results on antibody tests, we should pursue additional virus-specific tests (such as viral load). HIV-infected individuals can be seronegative for a number of reasons, including seroreversion, late seroconversion, evaluation during the window period, and defects in the immune system that prevent development of a humoral response to infection. Also notable in this report is the finding that a genetically uniform population of CCR5-tropic variants can cause rapidly progressive, fatal HIV infection, a course generally thought to be associated with CXCR4-expressing variants.

— Sonia Nagy Chimienti, MD

Published in Journal Watch HIV/AIDS Clinical Care November 23, 2009 (http://aids-clinical-care.jwatch.org/cgi/content/full/2009/1123/1)

Actually, who will really bother about the above ‘reminder’? There have been at least 25 cases and probably countless cases discounted by conclusive tests due to official stand around the world.

AIDS. 2010 Jun 19;24(10):1407-14.
Seronegative HIV-1 infection: a review of the literature.
Spivak AM, Sydnor ER, Blankson JN, Gallant JE.

Johns Hopkins School of Medicine, Division of Infectious Diseases, Baltimore, Maryland 21287, USA.

Abstract
HIV-1-specific antibodies can be detected in HIV-1-positive patients within weeks of primary infection. Rare cases have been reported of patients who are persistently seronegative despite evidence of HIV-1 infection. We present a retrospective review of the clinical, virologic and immunologic characteristics of 25 persistently seronegative patients whose cases have been published to date and postulate a biologic mechanism for this phenomenon.  (http://www.ncbi.nlm.nih.gov/pubmed/20467287)

One might be having some immune defects that they cannot react to the virus, and a ‘reconstruction’ of the immune system is needed. The problem is… how would this be done in Singapore? In Singapore, tests would be conclusive after 12 weeks with fourth generation test and the only reason for non-seroconversion is you take PEP drugs…

2010: Spivak Adam M; Brennan Tim P; O’Connell Karen A; Sydnor Emily; Williams Thomas M; Siliciano Robert F; Gallant Joel E; Blankson Joel N

A case of seronegative HIV-1 infection.

The Journal of infectious diseases 2010;201(3):341-5.

Patients infected with human immunodeficiency virus type 1 (HIV-1) typically seroconvert within weeks of primary infection. In rare cases, patients do not develop antibodies against HIV-1 despite demonstrable infection. We describe here a human leukocyte antigen (HLA)-B*5802-positive individual who presented with acquired immune deficiency syndrome despite repeatedly negative HIV-1 antibody screening test results. Phylogenetic analysis of env clones revealed little sequence diversity, and weak HIV-1-specific CD8(+) T cell responses were present to Gag epitopes. The patient seroconverted after immune reconstitution during receipt of highly active antiretroviral therapy. Lack of an antibody response to HIV-1 is rare and appears to be due to a defect in HIV-1-specific immunity rather than infection with attenuated virus. (http://www.biomedexperts.com/Abstract.bme/20039801/A_case_of_seronegative_HIV-1_infection)

This is the one (below) that is making things very disturbing… The point is, I read with sadness with imaginable suffering of the patient with an infection gone unnoted for so long… despite tell-tale readings and symptons.

Volume 15, Number 1–January 2009
Letter
Fatal HIV Encephalitis in HIV-Seronegative Patients
Troy M. Martin and Josiah D. Rich
Author affiliations: Brown University School of Medicine, Providence, Rhode Island, USA

Suggested citation for this article

To the Editor: Acute encephalitis is rarely seen in patients infected with HIV. In addition, HIV in patients who are seronegative is extremely rare, particularly in the setting of current screening ELISAs. We report a case of encephalitis and HIV in the same patient, which resulted in death.

A 44-year-old Caucasian woman sought treatment at our hospital with a 1-week history of fever, unsteady gait, and progressive confusion. Her medical history included hypothyroidism, depression, and chronic alcohol abuse. The patient’s first test for HIV was negative at 19 and 12 months prior to admission during routine intake screening for jail inmates (Abbott HIV AB HIV-1/ HIV-2 [rDNA] enzyme immunoassay [EIA] kit; Abbott Laboratories, Abbott Park, IL, USA). Six months before admission, the patient had a viral exanthem of blistering rash on her lips, palate, and chest. Two weeks later, she had oral thrush and a leukocyte count of 1,700 cells/μL. An HIV ELISA result was negative. Three months before admission, she was admitted to a different hospital for weakness, abdominal pain, intermittent fever, diarrhea, persistent oral candidiasis, and ethanol withdrawal. She had leukopenia and thrombocytopenia. A fourth HIV ELISA result was negative. The patient had been admitted to our hospital one week before the current admission with symptoms of fever, confusion, and urinary tract infection. Lumbar puncture showed an elevated protein level (106 mg/dL). A fifth HIV test result 6 days before most recent admission was negative. Five days before admission, she had been discharged to a rehabilitation facility. (Shit!? They discharged her with all those readings?!)

On this hospitalization, she had fatigue, headache, disequilibrium, dysarthria, and blurred vision. Initial examination showed fever of 101.3°F, poor word recall, and a wide-based gait. Laboratory tests showed mild anemia and a leukocyte count of 2 × 103 cells/μL.

Over the next few days the patient’s fever persisted and her mental status fluctuated. Tests on hospital day 2 showed a CD4 count of 101/mL (16.9%). Magnetic resonance imaging (MRI) of the brain showed diffuse symmetric white matter disease (Figure, panel A). Samples sent on hospital day 9 eventually showed wild-type HIV with a viral load >500,000 copies/mL. Repeat cerebrospinal fluid (CSF) test results were negative for cryptoccocus antigen, and PCR results were negative for cytomegalovirus, herpes simplex virus (HSV), and JC polyoma virus. The next day a sixth HIV ELISA result was negative. The serum level of HIV p24 antigen was 202 pg/mL.

On hospital day 13, she was started on zidovidine, lamuvidine, didanosine, and nevirapine. Within 24 hours, seizures and catatonia developed in the patient. An electroencephalogram showed diffuse wave form slowing. A repeat MRI showed worsened white matter disease (Figure, panel B). The result of a seventh HIV screening ELISA performed on hospital day 15 was negative. Two days later, the HIV viral load was 241,789 copies/mL. On hospital day 19, her serum levels were within normal limits: immunoglobulin (Ig) M level (164 mg/dL), IgG level (1,440 mg/dL), a 3× normal IgA level (1,060 mg/dL), and no oligoproteins. The CSF had an IgG level >10× normal (72 mg/dL), elevated IgG levels for HSV1 (1:160) and HSV2 (1:40), was negative for virus culture, and showed a negative rPCR result for JC polyoma virus. On hospital day 23, the eighth HIV ELISA result was negative. The Abbott HIVAB HIV-1/HIV-2 (rDNA) EIA was used throughout the hospitalization. On hospital day 24, supportive care was withdrawn and the patient died. Throughout her hospitalization, blood, urine, and CSF cultures remained sterile.

Autopsy showed acute HIV encephalopathy and cerebral vasculopathy. The findings included multifocal microglial nodules, perivascular inflammatory cells, vasculopathy with mural fibrosis and perivascular hemosiderin deposition, degeneration of the central white matter, and neuronal apoptosis (Figure, panel C). She also had Pneumocytis jiroveci pneumonia and hepatosteatosis without cirrhosis.

There are several possible explanations for the patient’s HIV seroconversion failure. The first explanation is that the patient was subacutely infected but had a retarded humoral response. Delayed seroconversion has been documented up to 42 months after infection, but this seems unlikely with current ultrasensitive assays. Another possibility is that she was infected with a strain undetectable by screening ELISAs, such as HIV-1 Group N or a rare Group M subtype recombinant variant. This hypothesis also seems unlikely because of the rarity and geographic distribution of these strains. A third possibility is transient seroconversion with reversion to seronegative status. However, given the number and frequency of screening tests in this case, even transient seroconversion would probably have been detected. Another hypothesis, one consistent with the patient’s rapid demise, is infection with a particularly virulent HIV variant, which led to rapid immunocompromise and failure of seroconversion. Such infections have been observed in rapid progressors, in which CD4+ T-cell depletion is so swift that B cells receive no T-cell help and are therefore not able to mount an effective immune response. In addition, chronic alcoholism may have contributed to immune failure and a rapidly progressive disease course.

This case raises several disturbing and interesting questions and possible avenues for future research. The diagnosis of acute HIV encephalopathy with a CD4 count of 100 cells/μL raises the likelihood that this patient was infected with at least 1 strain containing particularly neurotropic properties, possibly with X4 or R5X4 tropism, or that her brain was particularly primed for HIV-induced damage. Understanding the neurotropic properties of different strains of HIV may help prevent similar adverse outcomes in other patients.(http://www.cdc.gov/eid/content/15/1/129.htm)

Am I… another case as similar as the above…? Here, India has some interesting cases. It seems that we are really living in a box of mystery.

Seronegative HIV-2 carriers in India
S Kageyama, J K Maniar, M Iwasaki, J Zhang, D G Saple, H Tsuchie, A Tanabe-Tochikura, K Taniguchi, K Shiraki and T Kurimura

The discordant cases of seronegative, but culture and proviral HIV-2 DNA positive were found in Mumbai, India. This was corroborated by the successful isolation of HIV-2-RNA in culture medium, HIV-2 cDNA sequence determination and the detection of the antigen. The sequence of the isolated HIV-2 genomic RNA does not seem to be altered to the extent that the change will alter antibody binding. Furthermore, antibody from the same individual (even at 8 months from initial sampling) from whom HIV-2 was isolated did not react with the antigen of this strain. Those evidences imply that extremely low or non-production of the antibody may be due to suboptimal immune stimulation due to extremely slow HIV-2 replication. This low virus-load may be responsible for the negative antibody results in the HIV-2 carriers. (http://ijsa.rsmjournals.com/cgi/content/abstract/11/1/31)

If you ever talked to an ‘expert’ or counsellor in Singapore, they will likely tell you all those international sources, professionals and medical records online are bullshits and unreliable. Basically, HIV is evolving very fast, and the only way to be certain is to do precise testing. Many would have gone undetected and be spreading this infectious disease with sweeping judgements which should be very lethal. There are plenty of other cases of which seroconversions have been negative even with the use of fourth generation test kits. There are many reasons for failed seroconversion, but a patient knows his or her condition best.

Never put others at risk… if the specialists refuse to do further investigations and you are feeling like shit… although they will tell you HIV won’t give you headaches and this and that, you never know.

University of Minnesota has successfully cured HIV infection in mice. So the world is now waiting for Mansky and team to produce the pills for clinical trials, and hopefully it could be fast-tracked by FDA.

Last but not least, a miracle piece:

After someone is infected with HIV, blood tests can detect antibodies to the virus, even if they never had any symptoms of their infection. This is called HIV seroconversion (converting from HIV negative to HIV positive by blood testing), and usually occurs within 3 months of exposure, but on rare occasions can by delayed up to a year after infection.

Following the initial infection, there may be no further evidence of illness for the next 10 years. This stage is called asymptomatic HIV infection.

Acute HIV infection can, but does not always, progress to early symptomatic HIV infection and to advanced HIV disease (AIDS). However, the vast majority of patients do ultimately progress to AIDS. To date there are a small number of people who have tested positive for HIV, but later no longer test positive and have no signs of disease. Although this is relatively rare, it provides evidence that the human body may be capable of removing the disease. These people are being carefully watched and studied.

HIV has spread throughout the world. Higher numbers of people with the disease are found in large metropolitan centers, inner cities, and among certain populations with high-risk behaviors. (http://www.righthealth.com/topic/Seroconversion_Hiv/overview/adam20?fdid=Adamv2_000604)

It’s not exactly hard to understand why we have a ‘miracle’ here. This article is said to be  doctor-reviewed, and while there is no known or official cure yet, the article suggests of people who could have cured themselves. Note the plural used, it’s ‘people’.

[Transmission Myths] Despite current specialists suggesting that oral sex has low risk… previously, it was suggested that oral sex had NO risk, and even earlier it was thought HIV was only a disease among gays… The truth is HIV has as high a risk in oral sex as in penatrative sex. This is due to the fact that your mouth has membrance the like of a cunt’s, and the penis tip is also thin enough to absorb the fat virus. Ejeculation will bring about a fluid exchange for oral sex. So… decide for yourselves.

Sucking nipples also carries a risk. Unknown to many, women not only produce milk but also other body fluids in random. Hence sucking nipples could be a mode of transmission.

And despite the fact that HIV doesn’t stay alive very well outside the human body… yet it can be ‘alive’ for days and even weeks in (eg) syrings. So sharp objects could host the virus for some time. While the saliva has many enzymes which could even kill HIV, but there has been a known case of man been bitten by an infected and being infected with HIV. Saliva contains the virus, and saliva can infect people. Hence oral sex is never never low risk.

Two Malaysians made news in Singapore recently to be infected with HIV without sex or drug abuse… Doctors suspected dental care could be a reason (what if they did have sex? It’d end up a false source placed into the figure). But the point is, don’t believe in those transmission myths… Usually, in Africa, a family member infected with HIV also represents a family of infected. Is HIV contagious? Yes, it is. The myth of it is ok to eat together must be heavily doubted… You must not share drinks nor food, and you must be very careful when the infected sneezes… Yes, even your eyes can welcome HIV.

Herpes Simplex Type 1 & 2

This is a particularly dangerous viral infection in Singapore because Singapore specialists are extremely low-guarded and mostly not updated especially when it comes to family clinics, and antiviral drugs are to be prescribed by them. The unusual issue about this virus is in Sweden almost everyone is infected with this virus, and in Turkey… almost no one is not infected. This is a very contagious virus whereby 50% or more got it when they were babies… where fingers were touching things and placed then in the mouths, and many nail-biters and team-sports players are infected unknowingly. Professions such as teaching and medical care workers are at high risks.

The test for type specific antibodies may not be accurate if the virus remains latent upon initial infection.

Herpes Simplex Type 1 differs from type 2 in that it has a tendency of lower recurrence in general and the prefered location of activities. However, type 1 and type 2 can infect any parts of the body and even with the presence of antibodies you can still reinfect yourself with either versions in another part of the body. Hence, I am arguing against wasting big money developing vaccines due to immune response instead of developing a cure. The other issue is, whether a cure is more profitable or a treatment?

Since HSV1 and 2 are so contagious, even treated by a cure, the market will still be there with reinfected cases. Whereas for a treatment, many are going loose on antivirals because in general blisters or cold sores ain’t a big issue unless they happen on the genitals.

HSV1 has been misunderstood as the ‘better boy’, but updated researches on this virus shows that HSV1 is the killer as compared to HSV2 because it has a higher frequency of travelling to sites of the brains and the eyes, and herpticum can occur to attack the skin and various organs. Despite what your specialists would suggest that HSV infection is no big deal…
Herpes facts:

*Genital herpes in the United States increased in prevalence by 30 percent in the 1980s and 1990s, according to one study. Between one in five and one in six American adults are infected with genital herpes, but up to 90 percent of people are unaware they are infected.

*Herpes is transmitted through direct skin-to-skin contact, when a contagious area comes into contact with a tiny break in the skin or mucus-membrane tissues, primarily the mouth and the genitals.

*Most people have mild symptoms or no symptoms. Classic symptoms are sores that resemble small pimples or blisters that eventually crust over and finally scab like a small cut. The lesions may take two to four weeks to fully heal.

*While rarely leading to other health-related complications, a diagnosis of genital herpes can cause embarrassment and anxiety and lead to social isolation. Herpes outbreaks and the risk of transmission can be reduced by the frequent use of oral anti-viral medicines such as Valtrex, Famvir and Zovirax.

*Herpes can be spread when symptoms are present and not present.

*Regular condom use can decrease the rate of transmission.

*There are no documented cases of a person getting genital herpes from an inanimate object, such as a toilet seat, bathtub or towel. The herpes virus is fragile and doesn’t live a long time on such surfaces.

*Blood tests and other tests are available to diagnose herpes.

*Medical costs associated with genital herpes in the United States come to somewhere between $207 million and $984 million a year, according to the most recent estimates, which are about 10 years old.

*An estimated 5,000 people die worldwide from herpes simplex virus-2 and herpes simplex virus-1. Babies, who can acquire genital herpes from their mothers in childbirth, can become extremely ill and suffer brain damage as a result of genital herpes infection.

*Herpes ulcers can enhance the transmission of human immunodeficiency virus, which causes acquired immune deficiency syndrome, or AIDS.

Sources: American Social Health Association (http://www.ashastd.org), SIU School of Medicine scientist William Halford and State Journal-Register research. (http://herpesvaccineresearch.com/)

Despite Singapore specialists’ carelessness on HSV infections and the convenient dismissal of it being anything but a nuisance plus dismissing online resources as bullshitting, but SIU scientist obviously would not agree. And the most dangerous issue in Singapore is… Singaporeans would not have the drugs ready in wait in case the organs are attacked, and local specialists usually will not dispense medication unless they see the attack… And how are they going to ‘see’ your organs attacked? Which is something the ministry of health should enlighten the patients.

Singapore specialists will also not inform patients in general about the diet’s association with the disease. Lysine and arginine play very active roles in deciding disease progression. For a list of food considerations, please refer to http://www.herpes-coldsores.com/diet_and_nutrition_with_herpes.htm . For instance, try not to eat corn flakes without milk. Herpes Simplex patients should also avoid the sun, the wind, stress, and other triggers which may weaken your health. A poor GI condition will aggravate HSV infection as well as extreme temperature, burns and… patients should not have a late night sleep.

Obviously, military is a very bad career option for patients.

Currently there are many updated researches on HSV infections, and cure development from a David C Bloom from the University of Florida has reached animal trial where previous trials have been positive. A Prof Cullen is also developing a cure, but Cullen seems to be short of money and has not even started testing in mice. An artificial antibody called Bavituximab that is in human trial actually possibly helps curing by attaching itself to the PS of the infected cells, marking the cells for immune response. This PS is expressed in herpes, HIV and Hepatitis C infections alongside with other influenza  infections. If Prof Bloom’s hammerhead ribozymes approach succeeds, it is estimated that a cure would be around in two years for HSV infections.

HSV is also linked to many chronic and fatal diseases. The most dangerous part about HSV1 is complications… Like Chicken Pox, Chicken Pox can also kill… but rarely so.

The definition of HSV1 as an STD can be very misleading because many children who can’t be sexually active are also infected. It is updated that Chicken Pox never enters true latency, and HSV infections constantly maintains an inflammation in the body. Once activated, the first outbreak of HSV will be generally harsher as the body only begins to produce antibodies against the infection. Recurrence generally become less problematic and mysteriously even dies out in some individuals. Compounding to the theory that latency is established due to a built up force of patrolling antibodies, I suggest that the virus could at the nervous system mutate in a way to fit in to the body condition of certain individuals.

One interesting note about this infection is… once it got into the ganglion nerve cells, the cells are known to become ‘immortal’… which is, the cells will always go on functioning… There is a thought… what if we infect humans with mutated HSV without all the diseased genes… Since virus cannot enter another host cell which is already occupied by another virus… would that be a super vaccination? Once infected, the virus may lie dormant… and my advise is… keep it that way, because once it is activated, the virus will start outbreaks (replications) and you don’t really like recurrences even if there are no symptoms.

Due to the fact that genital herpes recur more frequently, because the nerves at the lower body are disturbed more frequently by motions, hormones, and such than the nerves at the ear for HSV1, it is paramount that the infected prepare Zinc Oxide and refrain from sexual activites such as mustabation. Dental surgery also stirs HSV1 outbreaks in a different manner. And do not touch your cunt or dick and rub elsewhere…

Updated 28 Dec 2010: The long mystery of why HSV1 infected never have recurrence later in life (after some years) regardless of immune condition has through recent discovery to be the infection possibly been cleared out by the immune system, indicating a self-cure. However, this research is only being found in mice experiment. It also, however, supports Luc English’s discovery of a combative immune response attacking HSV1 infected cells.

HPV

It is said to be incurable, but similar to HSV infection and even in the case of HIV infection for an Andrew Stimpson, immune response is the only way to ‘cure’ the infection. Typically, HPV produces warts by infecting the mucosal layer of a person in the mouth, in anus, in the virgina, at the fingers, neck, eye lids, lips… anyway. And the sorry issue is, there are HPVs everywhere… in another’s finger nails, palms, and even towels or bedsheets… There is no way a person won’t get infected with HPV in his or her lifetime. Some HPV strains causes cancers… but remember, your immune system is there also to deal with cancers happening daily.

There are two ways to deal with HPV warts… One, you remove them physical by surgery or treatment. Or you risk reinfection to other body parts by leaving the warts around and hoping for your immune response to clear out the infection. The problem about the human body is… if it is not serious, immune response usually slacks… That’s why HSV usually are ‘treated’ by the immune system when it causes problem and not bothered with when it is latent hiding in host cells.

What most specialists will not tell you outright at first… provided you ask, is that HPV, like any other influenza and diseases including cancers, could be cleared out by your immune system over time. The sorry issue is, it could take an average of two years.  And you could have it infecting someone else or yourselves, and it could be causing cancerous growths… but when the body has developed the immune capability to clear out the infection, it’d be easier to clear out potential warts faster, and prevent warts from appearing again because the virus is being cleared out.

Why would it not be recommended to physically try to remove warts? That’s because till the immune system detects the infection causing abnormalies, thymus usually won’t do anything. In fact, usually inflammation will increase the attention of the immune system towards an infection, which is why it is always prefered for the immune system to learn to be able to fight and clear the warts. But of course, there is always a risk of… what if the immune system of yours can’t ever learn?


[It’s not courage that’s making me point blank that Scope is chronically infected#1. It’s merely personality. And there goes my love-life, and the seek for true love, which is probably an end of failure even if the search goes on. I definitely believe I am dying… It has been hell since August. My lymph node under the left chin swells since mid Sep 2010 till now… The headaches were killing me… It’s really quite an horrifying experience waiting to die. The discovery of TRIM21 points to possible immune response to rid ourselves of infections even in infected cells… but how? The local medical world so far is treating what I have been diagnosed as more of a nuisance infection… though uncurable at the moment, they think it’s not serious. Mdm Alison probably wasn’t thinking that… I am going to kiss her daughter when she said I can still have a life, have sex, have a woman to make me babies… And the joke is… I don’t even know where and when exactly I got this infection!? I could have gotten it when I was a virgin teenager! Anxiety over possible HIV infection plus Cat and many things probably killed the immune system and… I am now dying. I probably can still work, but… I am banning myself from women… Life is not going to be easy for a man to do without banging women. But… life isn’t going to easy for me to do with love. I can’t find a woman, I can’t find love, banging or no banging~]

Summary

For HIV, it is very likely a cure is coming in about 5 years, but the false negative situations are freaking me out. Basically, Abzymes are in the development, Mansky’s drugs combination is as well in the making and Hebrew scientists have discovered crucial method of singling out infected cells for the attack leaving healthy cells unharmed. For HSV, generally, Bavituximab has been known to be effective to PS expressing infected cells by Herpes family infection, and there is impatience from sufferers of herpes to have bavituximab quickly available in the market.

Here’s the myth again… it’s a myth that you would be clear of HIV, HSV and HPV infections if you abstain from sex. But it is true that sex increases the risk critically for infection especially for HIV.

Seronegative HIV infected could be due to autoimmune issues caused collectively by infection of CMV, EPV and HSV where the updated studies show together, they decrease killer cells in our system substantially and EBV is known to infect B-cells and cause autoimmune issues.

While the viral infections of the herpes family is well-spread, the world awaits impatiently for Bavituximab to enter the market to cleanse our bodies. While a cure is under development for HSV1, maintaining a healthy lifestyle is always an issue with or without known diseases.

I hope this section will help those facing challenges in life dealing with optimistic doctors and needing to convince the military.

#1 Stigma is not what I am concerned with because this infection affects probably a majority of world population such as Chicken Pox does… But… I have to assume infection rate in Singapore is pretty small, and like Chicken Pox… this infection can kill despite it’s rare happenings.  Someone said, it’s not hard to find a woman carrying this infection in some countries, but I am not about going to ask on the streets who are also infected… Nor do I trust myself wanting to be infected with another variant of infection. Yeah, they said you can’t be infected twice… Fuck lah~ I believe, however, that a cure is coming soon, or rather… I’d cure myself soon if… it doesn’t kill me. I simply don’t know how a civilisation that is about 100% infected could have been living with all the adverse factors around their homes like nothing ever happened.

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