*Edit Title* Louisiana what’s going on - 1 & 3 GET TESTED!

Doctor checking in. Worked in an HIV clinic and specialty pharmacy in Chelsea NYC as well as in the Bronx. So if you guys have any questions I’ll gladly educate.

A lot of the stuff being talked about here is true, some obviously isn’t. With that said, with the medications currently available you can live a normal life being HIV+. With the Medicaid and Medicare services available for those with HIV these super expensive medications have less than a $5 monthly copay.

Despite your heath insurance,
your sexual preference, and even the slim chance of contracting HIV through unprotected sex (highest chance through anal sex due to rectum ruptures and closer contact with blood) just strap up. Yes, most of my patients were homosexual black men or drug needle users, but I’ve had some very attractive female patients with the virus as well. Just strap up because you never know who has it.
 
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Just looking at the numbers the majority of homosexuals are white, yet a predominantly black city is the hot spot for HIV .... right....
 
ballinsam23 ballinsam23

Thanks for your input. You mind explicitly laying out what HIV + per the definition of a virus, how it is medically determined that someone has the disease?


dcallamerican said:
It used to be DC. When DC was 98% Black, we were getting all the world records for infected folks with AIDS/HIV.

Once Atlanta became the black capital of the world, they have been pushing that label
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The devils in the details. Earlier in the post I laid several things that could cause false positives, among them “Natural Occuring Antibodies and Healthy individuals as result of POORLY UNDERSTOOD cross reactions.” I’ve yet to see anyone address this. Since the word conspiracy gets people bent out of shape, at its simplest that’s poor science. How are we hitting people with death sentences and prescribing medicine for stuff they don’t even truly understand.

People like Rusty will act high and mighty because someone didn’t vote, and say it’s the reason we’re dealing with people like Trump yet disregard the total package that comes along with white supremacy. Insidious biochemical warfare has always been part of that package. How’s it going down this generation?
 
C.Magneto C.Magneto Which of the following are you suggesting?

1. If you test positive for HIV, do not take the prescribed medication cause it’s a false positive.
2. If you text positive for HIV, Don’t take the prescribed medication because the medication will kill you, not the virus that leads to AIDS.
3. Don’t get tested for HIV.
4. Other. If other, explain how you recommend proceeding if multiple tests suggest you’re HIV positive.
 
C.Magneto said:
Just looking at the numbers the majority of homosexuals are white.
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That chart would make sense, considering it’s directionally aligned with US population by race percentages....
 
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C.Magneto said:
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Just looking at the numbers the majority of homosexuals are white, yet a predominantly black city is the hot spot for HIV .... right....
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thats because there's a major of white people in da US, period... percentages wise? with Atlanta being da black gay capital of America, numbers are basically par for da course.
 
C.Magneto said:
Thanks for your input. You mind explicitly laying out what HIV + per the definition of a virus, how it is medically determined that someone has the disease?
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HIV+ basically means you have a virus that attacks your immune system and destroys CD4 (specifically T helper) cells. These T helper cells are needed to fight off infections and protect your body. They're basically the bullets in a gun. The HIV virus is a retrovirus so it makes copies of itself inside of these T helper cells and you're basically getting bullets that backfire and you can no longer protect yourself from opportunistic infections and other disease down the line.

HIV1 is the more common strain seen worldwide (mostly in the UK). HIV2 is most commonly seen in West Africa.

Depending on the setting (inpatient vs. outpatient) there are a bunch of diagnostic tests that can be done. ELISA, Western Blot, and even an at home testing kit (OraQuick) that are very accurate. I still recommend to get numerous diagnostic tests for a true positive. They test for specific HIV antibodies (IgG, IgM) or the p24 antigen that can be found through oral mucus, blood, urine samples.

The most important factors are CD4 count (basically an indicator of your immune function) and Viral Load (amount of virus in your blood). When patients are diagnosed with HIV they start on HAART therapy. If they are not diagnosed but are in close contact (accidental needle poke, men having sex with other gay men, etc) they can still be on prophylactic therapy (Truvada).

If someone contracts the virus and is + they'll go through different stages. Stage 1 is usually an acute phase where in the first 3-6 months you'll have fever like symptoms (weight loss, body pain, rash, mono, etc). As months and years go by, your viral load increases and your CD4 count decreases. All HIV meds (HAART therapy) are there to decrease the viral load to less than 50 and increase your CD4 count. If you're not on HAART therapy your CD4 count keeps dropping and you can eventually get AIDS (CD4 count < 200). This typically takes years. Once your CD4 count is less than 200 you are now immunosuppressed and immunodeficient and can die from diseases such as tuberculosis, pneumocystis pneumonia, etc.
 
Don't use this as an excuse to not go to ATL. I head there at least once a year and all the baddest women I've seen I saw in ATL.

Strap up and you should be okay. Theres a large homosexual presence there which only skews the ratio drastically in your favor if you're hetero.
 
Chopper said:
That would make sense, considering it’s directionaly aligned with US population by race percentages....
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Good point, but then it begs the question why is it only an epidemic when it comes to minorities. I don’t see whites talking about their down-low husbands, or how they need to strapped up in Portland cause it’s foul out there.

As far as treatment, it’s a case by case scenario.

I urge people to do their research and come to their own conclusion.

Personally, I don’t mess with western medicine unless it’s an emergency/trauma situation.

ballinsam23 ballinsam23 Thanks for the insight. But I feel my point is still being made. You’re not testing for a virus in the traditional sense, You’re testing for a CD4 count. As I laid out earlier there’s multiple factors and lifestyles that could lead to a lower CD4 count. For example, and this is particularly why you see homosexuals predominantly testing positive for HIV: They use poppers to relax the anal muscles. Continued use causes alkyl nitrite to compromise the immune system and brings about a lower CD4 count. If you’re looking under a microscope and hiv is cited as being there, when in actuality it’s a comprised CD4 cell you’re examining and you’re testing for an antibody level that fluctuates for a multitude of reasons, what are you left with that specifically points to a virus per the scientific definition? It’s the perfect set up if you’re waging war on a medically ignorant people. Set them up to live lifestyles that would automatically predispose them to having a lower CD4 account, say that because the lower CD4 count we believe you’re infected with this virus, and now big Pharma comes in with the medicine that you conveniently need for the rest of your life if it doesn’t kill you.
 
I see what you're saying and it has been brought up in the past. But in the end of the day it's still a retrovirus, not your typical virus. No question one of the most difficult to study. There are only 3 retroviruses that exist.

You're testing for antibodies (predominantly IgG). While the drugs and alkyl nitrite in theory may alter your immune system after prolonged use and can be a risk factor, it will not drop your CD4 count to levels less than 200 like HIV/AIDS can. Honestly, nothing will drop your CD4 count that low unless you're severely immunocompromised and immunodeficient. You can bring up Big Pharma all you want, that argument will always be there. In the end of the day if HIV patients want to live normal long lives they need to be on HAART therapy for the remainder of their life span.

Also, low income areas are statistically highest in HIV rates. I blame that more on actual drug and needle sharing use than MSM. Check this out...

"High rates of drug use have been documented among young men who have sex with men (YMSM). However, updated prevalence data are needed to understand current trends, especially for drug use before sex. We used baseline data from an HIV prevention trial to examine demographic differences in drug use (in general and before sex) among YMSM in Atlanta, Chicago, and NYC. Marijuana was the most commonly used drug, but alkyl nitrites ("poppers"), cocaine, and Ecstasy were also common. Drug use was more prevalent among older and White YMSM, and it was similar between cities, except use of poppers was higher in NYC. Our data generally support national prevention efforts."

Prevention is the key in health care.
 
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boxdok said:
This is a definite wake up call for me. I stay in Atlanta. I have been doing Team raw this whole year too. My last check up was September definitely need to do another one before the year is out. Good thing I just recently got in a serious relationship though, so I’m only messing with one chick.
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Oh you trippin trippin huh
 
There’s so many attractive women out here because the pickings are slim. A third of the brothers out here are gay, another third are living a lie and are under cover. The ones of us on the straight and narrow have to deal with unstable chicks cheating on they dudes cause they spending to much time at they “homeboys” crib and not showing them enough attention. I’ve met a lot of chicks who said they’ve dated down low men. AUTOMATIC 3 strikes. No dude likes condoms but I swear when I went for a checkup a month ago it was my first time getting checked in almost 2 years and I was SHOOK. Everything came back negative and I promised myself I’d never be in that state of debilitating paranoia ever again. Said I’d even quit the lamb skin joints too. Nothing but gold wrappers until a chick has my seed.
 
doublemesh96 said:
Quick question for all my melanated peoples, have any of you ever been to or know anyone who’s been to an aids funeral??? Cuz I don’t and they try and pin these statistics on us like it’s wild rampant and I call bs as far as these statistical claims are concerned.
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Didn't go to the funeral but a relative died of AIDS related complications.

I had a conversation recently and one of my family members thought you could only get HIV from gay sex.

So the stats don't really surprise me that much :smh:
 
ballinsam23 ballinsam23 If HIV does exist, it doesn't behave like a retro virus. It is said to hijack the cell membrane, replicate it self and then destroy the cell. This process continuously happens which allows for the propagation of the virus. Thus per the definition it would be behaving as a traditional virus. As you stated, its theoretically a retro virus which would mean it needs the cell to replicate itself so it can hijack the DNA and then replicate itself into RNA and emerge from the cell membrane and duplicate itself in that matter. That in itself is a conflicting idea. (It's a retro virus but behaves like a regular virus) In addition to this glaring contradiction,HIV has never met the scientific criteria to undoubtedly prove its existence: "To prove the existence of a virus you need to do three things. First culture cells and find a particle you think might be a virus. Obviously, at the very least, that particle should look like a virus. Second, you have to devise a method to get that particle on its own so you can take it to pieces and analyse precisely what makes it up. Then you need to prove the particle can make faithful copies of itself. In other words, that is can replicate." As I stated the devil is in the details. Most people aren't willing to, or afforded the luxury of understanding how these things work so they will take what is ever told to them as gospel because it plays on primal concepts such as sex, death, and quality of life.

As far as a 200 CD4 count you know at that point it has to do with AIDS more so then the actual presence of a virus. Everything has a tipping point. Consistently getting black out drunk in college for a few years may not cause liver failure, but a lifetime of drinking and the lifestyle that comes with it will. In regards to AIDS its no different, if you live a lifestyle that compromises your immune system consistently, eventually you're getting to reach a point of no return which allows the CD4 levels to get that low.
Dealing with the avg HIV patient, we both know people can and do Test Positive" for HIV with much a higher CD4 count then that and the doctor will recommend them starting the HAART treatment so it doesn't reach that level. Per the standard of western medicine rather then isolate the specific issue, it prescribes the patient a shotgun method of treatment often giving little concern to what other parts the body may be effected ( Chemo, Antibiotics, SSRI's, Mood Regulators etc all being prime examples of this approach) Saying that to say, HAART is not with out it's side effects either and the effects AZT has on the body have been well documented. Hence why I recommended people do their research and let them decide what approach is best for them.

In summation, at best HIV is a theory with a lot of glaring inconsistencies that seem to benefit the people who have practiced this type of warfare since they first stepped foot on this land. Scientifically speaking, If I tried to pull this off in college regarding any other topic I would get an F and torn to pieces when reviewed by my peers. If it weren't for the implications that came along with the HIV economy this would be no different.
 
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Another physician checking in. This thread reaks of the flat-earther and nut-job conspiracy mongers and millenial pseudo-philosophers. Please don't think that going to a top 10 school and taking "some pre-med classes" before failing organic chemistry and not getting into med school makes you somehow an expert in the field of virology.

Source: UpToDate (most widely used evidence based resource used by physicians in practice today)

The natural history and clinical features of HIV infection in adults and adolescents
Author:
Paul E Sax, MD
Section Editor:
Martin S Hirsch, MD
Deputy Editor:
Allyson Bloom, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2018. | This topic last updated: Jul 24, 2018.
INTRODUCTION — Since the original description in 1981 of an unusual cluster of cases of Pneumocystis carinii pneumonia and Kaposi sarcoma in previously healthy men who have sex with men, substantial advances in our understanding of the acquired immunodeficiency syndrome (AIDS) have been achieved. The identification of a cytopathic retrovirus in 1983 and development of a diagnostic serologic test for human immunodeficiency virus (HIV) in 1985 have served as the basis for developing improvements in diagnosis.

In addition, therapy was dramatically altered with the introduction of antiretroviral drugs in 1987 and revolutionized by combination antiretroviral therapy (ART) in 1996. In the three years following the introduction of effective ART, mortality, AIDS, AIDS-defining diagnoses, and hospitalizations all decreased 60 to 80 percent. The EuroSIDA study, comparing this early ART period with pre-ART and later ART (1998 to 2002) treatment periods, found a sustained decrease in mortality and progression to AIDS with ongoing ART [1]. Despite the absence of a cure, the natural history of the disease was radically changed, and now, certain patients with HIV infection without other significant comorbidities who are treated before significant immunosuppression can expect a life expectancy approaching that of the general population [2].

Despite these advances, it is still useful to review the natural history of HIV infection without ART and the classification of disease. Although modified from the initial case definition, the newer Centers for Disease Control and Prevention (CDC) classification system remains the cornerstone for diagnosing HIV and AIDS.

This topic reviews the case definition, stages, and natural history of HIV infection. The epidemiology of HIV infection, factors that influence the natural history of HIV infection, and the impact of ART on the natural history are discussed elsewhere. (See "Global epidemiology of HIV infection" and "Use and impact of antiretroviral therapy for HIV infection in resource-limited settings".)

CASE DEFINITION — Clarification of the case definition of HIV infection is important for surveillance and public health purposes. Organizations such as the Centers for Disease Control and Prevention (CDC) in the United States and the World Health Organization (WHO) have established case definitions to standardize the description of HIV infection cases. Although they reflect the clinical diagnostic evaluation for HIV infection, these case definitions are not intended to serve as the bases for clinical decisions in individual patients. The clinical diagnosis of HIV infection is discussed in detail elsewhere. (See "Screening and diagnostic testing for HIV infection", section on 'Testing algorithm'.)

CDC classification — The CDC laboratory criteria for the case definition of HIV infection include a positive result on a multitest algorithm (eg, a positive result on an antibody or combined antibody/antigen assay and a positive test on a supplemental test distinct from the first) or a positive HIV virologic test (table 1) [3]. This case definition is inclusive of testing algorithms that do not incorporate Western blot or immunofluorescent assays. In the United States, all HIV infections can be assumed to be with type 1 (HIV-1) unless specific testing has demonstrated infection with type 2 (HIV-2) or cannot distinguish the type. (See 'HIV-2 infection' below.)

The CDC case definition also classifies HIV infection based on the absolute CD4 cell count as stage 1 (CD4 cell count >500 cells/microL), 2 (CD4 cell count 200 to 499), or 3 (CD4 cell count <200 cells/microL). Criteria for stage 3 are also met by the presence of a stage 3 (ie, AIDS)-defining opportunistic illness (table 2). The classification system also includes stage 0 infection, which is defined as early infection (with a negative or indeterminate HIV test within 180 days prior to the first confirmed positive test) regardless of the CD4 cell count or presence of opportunistic illness.

WHO classification — The WHO case definition of HIV infection includes 1) a positive result on a HIV antibody test confirmed by a positive result on a second, different HIV antibody test and/or 2) a positive virologic test confirmed by a second virologic test [4]. The WHO classification system for staging established HIV infection uses both immunologic (table 3) or clinical (table 4) criteria.

OVERVIEW OF STAGES OF HIV INFECTION — HIV infection can be divided into the following stages:

●Viral transmission. (See 'Viral transmission' below.)

●Acute HIV infection (also called primary HIV infection or acute seroconversion syndrome, among other terms). (See 'Acute and early HIV infection' below.)

•Seroconversion describes the development of detectable antibodies, which generally occurs within the first several weeks after infection (depending on the antibody test used).

●Chronic HIV infection. (See 'Chronic HIV infection, without AIDS' below and 'AIDS and advanced HIV infection' below.)

•Asymptomatic.

•Early symptomatic HIV infection (previously known as AIDS-related complex [ARC] or Class B).

•AIDS characterized by a CD4 cell count <200 cells/microL or the presence of any AIDS-defining condition (table 5).

•Advanced HIV infection characterized by a CD4 cell count <50 cells/microL

VIRAL TRANSMISSION

Mode of acquisition — HIV infection is usually acquired through sexual intercourse, exposure to infected blood, or perinatal transmission. The mode of acquiring HIV infection was undetermined in 4 percent of the cases originally reported to the United States Centers for Disease Control and Prevention (CDC). A careful review of 32,497 cases, however, revealed that only 0.2 percent had no clearly defined risk factor.

The distribution of the modes of transmission of HIV infection varies in different countries. In resource-limited areas, vaginal sex is responsible for 70 to 80 percent of HIV infections, and perinatal transmission and injection drug use (IDU) for 5 to 10 percent each [5]. By contrast, in the United States and Western and Central Europe, male-to-male sexual contact is the most common route of HIV transmission. (See "Global epidemiology of HIV infection", section on 'Modes of transmission driving the epidemic'.)

Risk factors — Risk factors for HIV transmission include high viral load, certain sexual behaviors, presence of ulcerative sexually transmitted infections (STIs), and lack of circumcision, as well as certain host and genetic factors [6-8]. (See "HIV infection: Risk factors and prevention strategies", section on 'Risk factors for infection'.)

●Viral load – For all modes of transmission, a higher viral load is associated with a greater risk of transmission. This is reflected in models that suggest that a large proportion of HIV infections are transmitted by individuals with acute and early infection, a finding likely related to the high levels of viremia that are seen in the setting of acute infection [9]. (See "Acute and early HIV infection: Clinical manifestations and diagnosis" and "Acute and early HIV infection: Clinical manifestations and diagnosis", section on 'HIV RNA detection'.)

●Sexual behavior – The type of sexual exposure (eg, receptive anal intercourse versus receptive vaginal intercourse) and whether it was protected with condoms or not affects the risk of HIV transmission. In addition, other factors, such as the number of sexual partners or sex under the influence of recreational drugs also affect the risk. As an example, in a study of 3257 men who have sex with men (MSM) in six United States cities, risk factors for HIV acquisition included history of a large number of sexual partners, unprotected receptive anal sex with a partner with an unknown HIV serostatus, and use of nitrate inhalants [10].

●Sexually transmitted infections – The presence of other STIs also increases the risk of HIV acquisition, as demonstrated in a study of 174 monogamous Ugandan couples with discordant HIV serostatus [9,11]. The probability of transmission was approximately four times higher in patients with genital ulceration compared with those without. Multiple other studies have confirmed these results. (See "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection", section on 'HSV-2 and risk of HIV transmission' and "Syphilis in the HIV-infected patient", section on 'Epidemiology'.)

●Lack of circumcision – Several randomized trials have demonstrated a decreased risk of HIV acquisition with circumcision in heterosexual men [12-15]. In addition, lack of circumcision has been associated with risk of HIV transmission in cohorts of heterosexual couples and MSM [16].

●Genetic background – Similarity of human leukocyte antigen (HLA) class I alleles between HIV discordant couples may affect the risk of transmission (see "Human leukocyte antigens (HLA): A roadmap") by selecting for viral strains that are more likely to escape the immune containment of the uninfected partner. In a study of 125 initially serodiscordant couples with intracouple transmission, and 104 persistently serodiscordant couples, sharing of HLA-B alleles was associated with accelerated intracouple transmission of HIV after controlling for other variables (hazard ratio
 
(hazard ratio 2.23, 95% CI 1.52 to 3.26) [8].

ACUTE AND EARLY HIV INFECTION — Different terms, including acute, recent, primary, and early HIV infection, have been used in the literature to refer to variable intervals following initial infection with the virus. In this topic, we use the term "early HIV infection" to refer to the approximate six-month period following HIV acquisition. We use the term "acute HIV infection" to refer to the symptoms that frequently occur during early infection just after HIV is transmitted.

The following sections briefly discuss the stages and impact of acute and early infection on the natural history of HIV infection. The epidemiology, clinical manifestations, diagnosis, and management of acute and early HIV infection are discussed in detail elsewhere. (See "Acute and early HIV infection: Pathogenesis and epidemiology" and "Acute and early HIV infection: Clinical manifestations and diagnosis" and "Acute and early HIV infection: Treatment".)

Stages of early infection — The viral and immunologic dynamics following HIV transmission can be characterized using the Fiebig classification, which consists of six stages (table 6) [17]. Fiebig staging is typically used for research purposes. Detection of early HIV infection is facilitated by "fourth-generation tests" that detect HIV p24 antigen prior to seroconversion (ie, prior to Fiebig stage 3) [18,19]. In addition, moving towards confirmation testing with a second immunoassay instead of Western Blot testing also improves the likelihood of diagnosing HIV in the early stages. (See "Screening and diagnostic testing for HIV infection", section on 'Testing algorithm'.)

One advantage of recognizing early and acute HIV infection is that it allows early antiretroviral therapy (ART) initiation, which has several known and potential benefits. (See "Acute and early HIV infection: Treatment", section on 'Rationale for initiation of ART in early infection'.)

Clinical presentation — Symptomatic acute HIV infection is characterized by fever, lymphadenopathy, sore throat, rash, myalgia/arthralgia, diarrhea, and headache. A significant proportion of patients with early HIV infection will be asymptomatic. In early HIV infection, which is a period of rapid viral replication and infection of CD4 cells, the viral RNA level is typically very high; HIV RNA levels greater than 1 million copies/mL are not uncommon. Furthermore, the CD4 cell count can drop transiently. The clinical features of acute and early HIV infection are discussed in detail elsewhere. (See "Acute and early HIV infection: Clinical manifestations and diagnosis", section on 'Clinical features'.)

The presence of symptoms and a prolonged illness (>14 days) during early infection appear to correlate with more rapid progression to AIDS [20,21]. In one study, for example, the risk of progression to an AIDS-defining diagnosis within three years following seroconversion was substantially higher in those with acute symptoms lasting more than 14 days than in those who were asymptomatic or had only mild symptoms (78 versus 10 percent) [20]. (See "Acute and early HIV infection: Clinical manifestations and diagnosis", section on 'Signs and symptoms'.)

Seroconversion — Seroconversion refers to the development of detectable antibodies against HIV antigens. The timing of seroconversion following infection with HIV depends upon the sensitivity of the serologic test (table 7). As serologic tests are becoming more sensitive, most HIV-infected patients have documented seroconversion during early infection, ie, within the first several weeks after infection.

Viral set point establishment — By approximately six months of infection, plasma viremia has reached a steady state level (viral set point); cytotoxic CD8 cells play a critical role in achieving that equilibrium and preventing further decline in the CD4 cell compartment [22,23]. In a prospective study of 33 patients with early HIV-1 infection, those with higher frequencies of HIV envelope-specific memory CD8 cells had lower median plasma HIV RNA levels and a lower likelihood of progression to CD4 cell count <300 cells/microL at 18 months (20 versus 56 percent in patients with lower frequency CD8 cell responses) [23].

The viral set point level is closely associated with the rate of disease progression in the absence of ART; this level is highly variable [24-26]. As an example, in a prospective study of 218 female sex workers in Kenya, higher set point viremia, in addition to lower early CD4 cell counts and symptomatic acute HIV infection, predicted faster progression to death after a median follow-up period of over four years [25].

A small proportion of people who acquire HIV demonstrate transient virologic control early in infection without ART. In an analysis of 2176 patients with documented acquisition of HIV infection, 145 patients (7 percent) spontaneously controlled viremia [27]. Women, and those without symptoms at seroconversion, were more likely to achieve undetectable HIV RNA. Regardless, most of these individuals do not durably sustain HIV control, and become viremic, eventually experiencing disease progression. (See 'HIV controllers' below.)

CHRONIC HIV INFECTION, WITHOUT AIDS — The period of chronic HIV infection following early infection, seroconversion, and establishment of the viral set point, but prior to the development of severe immunosuppression, is characterized by relative stability of viral level and a progressive decline in CD4 cell count. The average time from HIV acquisition to a CD4 cell count <200 cells/microL is approximately eight to ten years.

Asymptomatic infection — During this stage, the majority of HIV-infected patients are asymptomatic. Nevertheless, even in the absence of major signs or symptoms, many HIV-infected patients have generalized lymphadenopathy on exam.

"Persistent generalized lymphadenopathy" (PGL) is defined as enlarged lymph nodes involving at least two noncontiguous sites other than inguinal nodes for more than three to six months without an alternative explanation and was described early in the history of HIV as a common finding in otherwise healthy individuals with HIV infection [28]. The lymph nodes in such patients are generally symmetrical, modestly enlarged, mobile, painless, rubbery, and located in the cervical, submandibular, occipital, and axillary chains [29]. In the HIV-infected patient without severe immunosuppression or other clinical symptoms, further evaluation for the etiology of symmetrical lymphadenopathy is generally not warranted.

Symptomatic infection — Most HIV-infected patients remain asymptomatic, apart from possible generalized lymphadenopathy, during chronic infection prior to the development of severe immunosuppression (eg, CD4 cell count <200 cells/microL) (see 'Asymptomatic infection' above). However, certain clinical syndromes are seen with greater frequency and severity in the setting of HIV infection, particularly as the CD4 cell count decreases (table 8).

Although most of these HIV-associated complications occur or worsen with severe immunosuppression, many can occur at CD4 cell counts >200 cells/microL. As an example, in a study of over 7500 HIV-infected individuals from various urban sites in the United States, among those with a CD4 cell count 200 to 499 cells/microL, thrush was reported in 21.3 percent, oral hairy leukoplakia in 9.2 percent, herpes zoster in 6.7 percent, peripheral neuropathy in 3.7 percent, and idiopathic thrombocytopenia purpura in 2.6 percent [30]. Even among those with a CD4 cell count >500 cells/microL, thrush was reported in 11 percent. Recurrent or persistent candidal vulvovaginitis and cervical dysplasia were reported at similar frequencies among women who had CD4 cell counts <200 cells/microL or between 200 and 499 cells/microL.

Many of the signs and symptoms described in HIV infection without severe immunosuppression involve the skin or mucous membranes. In addition to recurrent or persistent oropharyngeal or vulvovaginal candidiasis (picture 1) and oral hairy leukoplakia (picture 2), seborrheic dermatitis (picture 3) is a common early finding of HIV infection. Bacterial folliculitis, particularly due to Staphylococcus aureus, is also common. The emergence of community-acquired methicillin S. aureus (MRSA) has disproportionately affected HIV-infected individuals, who appear to have a higher burden of colonization with MRSA compared with the uninfected [31,32]. In addition, the manifestations of herpes simplex virus (HSV), varicella zoster virus (VZV), and human papillomavirus virus (HPV) infections are often more severe (eg, with recurrences or more rapid progression) in the setting of HIV infection.

Other infections also occur with greater frequency in the setting of HIV infection, even in the absence of AIDS, including Streptococcus pneumoniae infection. Sexually transmitted infections (STIs), such as syphilis, and hepatitis B and C virus infections are also common because of shared routes of transmission, and they have more severe outcomes in HIV-infected individuals not receiving antiretroviral therapy (ART).

Some patients may have nonspecific constitutional symptoms, such as low-grade fevers, fatigue, and occasional night sweats prior to the onset of severe immunosuppression. Some symptoms may be attributable to non-infectious complications of HIV infection. These include cardiovascular, endocrine, neuropsychiatric, hematologic, and oncologic complications and are discussed in detail elsewhere. (See "Epidemiology of cardiovascular disease and risk factors in HIV-infected patients" and "Bone and calcium disorders in HIV-infected patients" and "Pituitary and adrenal gland dysfunction in HIV-infected patients" and "HIV-associated neurocognitive disorders: Epidemiology, clinical manifestations, and diagnosis" and "HIV infection and malignancy: Epidemiology and pathogenesis" and "Hematologic manifestations of HIV infection: Anemia" and "Hematologic manifestations of HIV infection: Thrombocytopenia and coagulation abnormalities".)

AIDS-defining illnesses (table 5 and table 4) may occasionally occur at CD4 cell counts >200 cells/microL. Their presence would, by definition, classify an individual as having AIDS. (See 'AIDS and advanced HIV infection' below.)

Viral dynamics and latency — Virologic studies in patients with asymptomatic HIV infection not on antiretroviral treatment show high rates of HIV replication and destruction of an average of 109 CD4 cells daily [33,34]. However, cell death and replacement are in near balance during this phase of the illness; thus, the decline in CD4 cell count is typically slow and a relatively steady state of viral load is achieved despite remarkably high turnover rates of HIV and CD4 cells. As an example, the HIV RNA levels are usually stable over time, with only rare changes exceeding 1 log [35].

The half-life of HIV in serum is approximately 1.2 days, about 24 hours intracellularly, and about six hours as extracellular virus. About 30 percent of the total body viral burden is turned over daily. Furthermore, 6 to 7 percent of the total CD4 cells turns over each day, and the entire supply of CD4 cells turns over every 15 days. The implication of these observations is that "AIDS is primarily a consequence of continuous, high-level replication of HIV, leading to virus and immune-mediated killing of CD4 lymphocytes" [34].

The lymphoid tissue serves as the major reservoir for HIV. Studies of the lymph nodes at this stage reveal high concentrations of extracellular HIV on the follicular dendritic cell processes within germinal centers and intracellular HIV predominantly in its latent form [36]. The viral burden in peripheral blood mononuclear cells is relatively low at this time. The lymph node architecture is disrupted and more HIV is released peripherally into the bloodstream as the disease progresses.

Eradication of this latent reservoir of HIV has been a focus of novel interventions aimed at curing the infection. However, diagnostic techniques are not yet sensitive enough to accurately confirm elimination of the viral reservoir. This was illustrated by a highly publicized study of two HIV-infected patients on antiretroviral therapy (ART) who underwent stem cell transplants for hematologic malignancies [37]. Following the transplants, while the patients continued ART, they had undetectable plasma viral levels and neither viral RNA nor proviral DNA was detectable in peripheral blood mononuclear cells or gut-associated lymphoid tissue from rectal samples, through sensitive quantitative polymerase chain reaction (PCR) and co-culture assays. However, following ART discontinuation to assess for potential viral eradication, both patients experienced symptomatic rebound viremia several months later. Phylogenetic analysis of the viral sequences in each patient suggested only a few latently infected cells contributed to the viral rebound.

CD4 cell count decline — Clinical studies show considerable variation between patients in CD4 cell count during this period, but the vast majority of patients experience progressive decline in the count. The rate of CD4 cell decline correlates with the viral burden. (See 'Viral set point establishment' above.)

In one study, the CD4 cell count decreased on average 4 percent per year per log copies/mL of HIV RNA [38]. Other factors, such as HIV subtype or host genetic background, are also associated with the pace of CD4 cell count decline [39,40].

Population-based studies of the natural history of HIV infection in men who have sex with men (MSM) have suggested that the mean CD4 cell count is approximately 1000 cells/microL prior to seroconversion and decreases to 780 cells/microL at six months following seroconversion and to 670 cells/microL at one year [41]. In a large prospective study of patients with well-estimated dates of HIV infection (the Concerted Action on Seroconversion to AIDS and Death in Europe, or CASCADE cohort), the estimated median time from infection to CD4 cell count decline to <500 cells/microL was 1.19 years [42]. Some patients have a substantially lower CD4 cell count at one year [43,44].

The rapid decline in peripheral CD4 cells in the early stages of HIV infection may reflect destruction of CD4 cells or a shift of CD4 cells from the peripheral blood to lymphatic tissue. After one year, the rate of CD4 cell decline slows, averaging about 50 cells/microL decrease per year, with a range of 30 to 90 cells/microL decrease per year [26,41,45-48]. Accordingly, there is a wide range of the time to progression to advanced immunosuppression (ie, CD4 cell count <200 cells/microL).

As with depletion of CD4 cells, humoral immunity wanes over time. B cells exhibit increased expression of markers of activation and proliferation [49]. In addition, in advanced HIV infection, B cells undergo terminal differentiation leading to increased immunoglobulin secretion [50], although many of these antibodies are nonspecific. This increased immunoglobulin level can be reflected on routine blood chemistries as an increased fraction of the total protein and can be a clue to undiagnosed HIV infection in a person not previously tested.

Immune activation — Some patients with long-term HIV infection that is virally suppressed on ART will develop evidence of premature aging (eg, cardiovascular disease, osteoporosis, cognitive dysfunction), which is thought related to chronic inflammation, immune activation, and immunosenescence [51,52]. (See "HIV infection in older adults", section on 'Immune activation'.)

AIDS AND ADVANCED HIV INFECTION

Definition — AIDS is the outcome of chronic HIV infection and consequent depletion of CD4 cells. It is defined as a CD4 cell count <200 cells/microL or the presence of any AIDS-defining condition (table 5) regardless of the CD4 cell count. (See 'AIDS defining conditions' below.)

The term advanced HIV infection is often used to refer to infection when the CD4 cell count is below 50 cells/microL.

When patients achieve immune reconstitution (eg, increase in the CD4 cell count >200 cells/microL) with antiretroviral therapy and have no AIDS defining conditions, they are no longer considered to have AIDS, only chronic HIV infection.

AIDS defining conditions — AIDS-defining conditions are opportunistic illnesses that occur more frequently or more severely because of immunosuppression. These include mainly opportunistic infections but also certain malignancies as well as conditions without clear alternative etiology thought to be related to uncontrolled HIV infection itself, such as wasting or encephalopathy. The AIDS-defining conditions listed by the Centers for Disease Control and Prevention (CDC) (table 5) and the World Health Organization (WHO) (table 4) criteria vary slightly.

Prior to introduction and widespread use of combination antiretroviral therapy (ART), AIDS-associated illnesses were the principal cause of morbidity and mortality associated with HIV infection. In a study of HIV-infected individuals seen at selected sites in the United States, AIDS-defining opportunistic illnesses were diagnosed in 10,658 men and 2324 women between 1992 and 1997 [53]. Pneumocystic jirovecii pneumonia was the most common initial opportunistic illness, occurring in 35.9 percent, followed by esophageal candidiasis, Kaposi sarcoma, wasting syndrome, and disseminated Mycobacterium avium infection (12.4, 11.6, 7.8, and 6.4 percent, respectively).

These opportunistic illnesses typically occur when the CD4 cell count has decreased <200 cells/microL, although they can less commonly occur at higher CD4 cell counts [54]. In an analysis of data from a well-described cohort of HIV-infected men who have sex with men (MSM) in the United States, the median CD4 count at the time of an AIDS-defining complication was 67 cells/microL, with approximately 10 percent of patients developing an AIDS-defining diagnosis with a CD4 count ≥200 cells/microL [55]. Certain opportunistic infections, such as disseminated M. avium infection and cytomegalovirus (CMV) disease, occur predominantly with a CD4 cell count <50 cells/microL. In the absence of ART, the median time to an AIDS-defining condition once the CD4 cell count is below 200 cells/microL is estimated at 12 to 18 months [56].

See the dedicated topic reviews for more details on the clinical presentation, diagnosis, and management of these opportunistic conditions in HIV-infected individuals.

Additional findings — Beyond the classic opportunistic illnesses that are categorized as AIDS-defining conditions (table 5 and table 4), a myriad of other findings are common in the setting of severe immunosuppression from HIV infection.

Findings that can occur at higher CD4 cell counts, such as mucocutaneous candidiasis, oral hairy leukoplakia, seborrheic dermatitis, and herpetic infections, occur with greater frequency when the CD4 cell count is below 200 cells/microL (see 'Symptomatic infection' above). Additional common dermatologic findings in AIDS include eosinophilic folliculitis, xerosis, prurigo nodularis. Molluscum contagiosum, bacillary angiomatosis, exacerbation of psoriasis, and severe scabies infections are also more frequent with severe immunosuppression. These are discussed in detail elsewhere. (See "HIV-associated eosinophilic folliculitis" and "Prurigo nodularis" and "Molluscum contagiosum" and "Epidemiology and clinical manifestations of Bartonella infections in HIV-infected patients".)

Hematologic aberrations are also very common in the setting of AIDS. Anemia, leukopenia, lymphopenia, or thrombocytopenia is found in over 40 percent of patients who present with CD4 cell count <200 cells/microL [57]. Significant lymphopenia can be a proxy for low CD4 cell counts in the setting of HIV infection when subset testing is not available. Polyclonal hypergammaglobulinemia is often observed. Many of these antibodies are nonspecific, which may partly explain the paradox between high circulating levels of immunoglobulins and an increased risk of bacterial infections (eg, recurrent pneumonia) that occurs in late-stage AIDS.

Prognosis — The median survival of patients with advanced HIV infection (CD4 cell count <50 cells/microL) is 12 to 18 months in the absence of ART [58-60]. Most patients who die of AIDS-related complications have CD4 cell counts in this range.

HIV CONTROLLERS — A minority of HIV-infected patients has very low or undetectable levels of HIV RNA, even using highly sensitive assays, in the absence of antiretroviral therapy (ART). They also maintain high CD4 cell counts for prolonged periods. These individuals are often referred to as "HIV controllers," with those without detectable virus referred to specifically as "non-viremic" or "elite" controllers. Non-viremic controllers represent a very small minority of HIV-infected individuals (approximately 1 in 300 patients), and the mechanisms that lead to spontaneous virologic control without treatment have been the subject of extensive investigation.

Nevertheless, despite lower levels of viral replication, HIV controllers still remain at increased risk for noninfectious complications of HIV, such as cardiovascular disease, compared with the seronegative population [61,62].

In non-viremic controllers, viral load suppression has been observed to be comparable to that seen in patients who are taking ART [63,64]. The median viral load in two cohorts of such patients was 2 copies/mL, although there were fluctuations over time [63,65-67]. Disease progression with CD4 cell count decline is unusual in elite controllers. This had not been documented in any of the 63 non-viremic controllers followed at the US National Institutes of Health (NIH) for a median of 19 years [66], but modest rates of disease progression have been reported in other cohorts [68,69].

Several factors may be responsible for spontaneous virologic control among individual non-viremic controllers, including infection with a defective HIV variant or host genetic polymorphisms. The human leukocyte antigen (HLA) class I allele most consistently associated with elite control of HIV is B57 [70]. One study evaluated cellular and humoral immune responses and host genetics in 64 non-viremic controllers, 50 persons with low levels of detectable viremia (<2000 copies/mL, "viremic controllers"), and additional patients with progressive infection [71]. This study showed that HIV gag protein was preferentially targeted by CD8 cell responses in non-viremic and viremic controllers compared with patients with progressive infection. The non-viremic controller group also had a higher frequency of HIV-specific CD4 and CD8 T-cells producing interferon gamma and interleukin-2 and a paucity of broadly cross-reactive neutralizing antibodies compared with the other two groups.

Additional studies, including viral and host genetic analyses, are underway. Information on studies of HIV controllers is available through the National Institutes of Health in the United States.

HIV-2 INFECTION — HIV-1 is the viral type that causes the vast majority of infection worldwide, although HIV-2 is an important cause of infection in certain regions of the world, such as West Africa or areas with historic ties to West Africa such as Portugal, Spain, and Goa, India. The general natural history of HIV-2 infection is similar to that of HIV-1 infection (ie, acute infection followed by prolonged asymptomatic chronic infection and ultimate immunosuppression with greater risk for additional infection and other comorbidities) but is characterized by lower levels of plasma virus, slower declines in the CD4 cell count, and a longer asymptomatic period of chronic infection. A detailed discussion of the natural history and clinical features of HIV-2 infection is found elsewhere. (See "Epidemiology, transmission, natural history, and pathogenesis of HIV-2 infection" and "Clinical manifestations and diagnosis of HIV-2 infection".)
 
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INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: HIV/AIDS (The Basics)" and "Patient education: Tests to monitor HIV (The Basics)")

SUMMARY

●Human immunodeficiency virus (HIV) infection can be divided into the following stages: viral transmission, acute HIV infection with seroconversion, and chronic HIV infection with or without evidence of the acquired immunodeficiency syndrome (AIDS). (See 'Overview of stages of HIV infection' above.)

●HIV infection is usually acquired through sexual intercourse, exposure to contaminated blood, or perinatal transmission. Risk factors for transmission include high viral load, certain sexual behaviors, presence of ulcerative sexually transmitted infections (STIs), lack of circumcision, and certain host and genetic factors. (See 'Viral transmission' above.)

●Symptomatic acute HIV infection is characterized by fever, lymphadenopathy, sore throat, rash, myalgia/arthralgia, and headache; however, a substantial proportion of patients with early HIV infection are asymptomatic. Early HIV infection is a period of rapid viral replication with typically very high viral RNA levels. By approximately six months of infection, plasma viremia has reached a steady state level. (See 'Acute and early HIV infection' above and "Acute and early HIV infection: Clinical manifestations and diagnosis".)

●The period of chronic HIV infection following early infection and seroconversion but prior to the development of severe immunosuppression is characterized by relative stability of viral levels and a progressive decline in CD4 cell count. The rate of CD4 cell decline correlates with the level of viremia. During this stage, the majority of HIV-infected patients are asymptomatic, although some may have generalized lymphadenopathy. However, certain HIV-associated clinical findings, such as thrush, seborrheic dermatitis, and susceptibility to herpesvirus and human papillomavirus (HPV) infections, bacterial pneumonia, and tuberculosis, frequently occur despite a CD4 cell count >200 cells/microL. (See 'Chronic HIV infection, without AIDS' above.)

●AIDS is defined by a CD4 cell count <200 cells/microL or the presence of any AIDS-defining condition (table 5) regardless of the CD4 cell count. (See 'AIDS and advanced HIV infection' above.)

●AIDS-defining conditions are opportunistic illnesses that occur more frequently or more severely in immunocompromised hosts. These include mainly opportunistic infections, such as Pneumocystis jirovecii pneumonia, toxoplasmosis, and disseminated Mycobacterium avium infection. Certain malignancies (Kaposi sarcoma, lymphoma), as well as conditions without clear alternative etiology thought to be related to uncontrolled HIV infection itself, such as wasting or encephalopathy, are also AIDS-defining conditions. (See 'AIDS defining conditions' above.)

●A minority of HIV-infected patients, despite not being on antiretroviral therapy (ART), has very low levels of viremia. They are considered HIV controllers. A subset of these patients are referred to as non-viremic controllers because they have no detectable viremia, even on ultrasensitive diagnostic testing. (See 'HIV controllers' above.)

●HIV-1 causes the vast majority of HIV infections worldwide, although HIV-2 is an important cause of infection in certain regions of the world, such as West Africa. Compared with HIV-1, HIV-2 infection is characterized by lower levels of plasma virus, slower declines in the CD4 cell count, and a longer asymptomatic period of chronic infection. (See "Epidemiology, transmission, natural history, and pathogenesis of HIV-2 infection" and "Clinical manifestations and diagnosis of HIV-2 infection" and "Treatment of HIV-2 infection".)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge John G Bartlett, MD, who contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.
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