Evaluation and management of acute HIV

OVERVIEW: What every practitioner needs to know

How does acute HIV infection usually manifest?

Acute HIV infection, typically occurring within weeks of an exposure to HIV-infected bodily fluids, represents the time in which a patient has high levels of plasma HIV RNA and an emerging humoral immune response with the development of detectable viral protein-specific antibodies. This period is frequently associated with an acute illness referred to as an acute retroviral syndrome (see Figure 1). This stage of HIV disease is also referred to as primary HIV infection. Often described as an “influenza-” or “mononucleosis-” like illness, the signs and symptoms are nonspecific and occur with variable frequency and severity. Symptoms can be minimal, very mild, or severe. Up-to-date screening tests are able to identify those with evidence of viremia in the absence of antibodies, regardless of presence of symptoms. For those presenting with symptoms, the more commonly described manifestations include:

Fever: Case series suggest this is the most frequent presenting symptom, although still only present in approximately 75% of patients.
Fatigue: This is a very common complaint, present in approximately 70% of patients.
Myalgia: This occurs in approximately 50% of patients.
Related Content
Skin rash: Rash is reported in approximately 50% of patients and has been variable in severity and presentation, often mimicking drug eruptions, secondary syphilis, and other viral exanthems.
Sore throat: Sore throat is a complaint in approximately 50% of cases, often associated with clinical evidence of pharyngitis with cervical adenopathy but usually without tonsillar exudates.
Lethargy/malaise: These are very nonspecific symptoms, but symptoms described in approximately 50% of patients.
Cervical adenopathy: This is present in approximately 30-40% of patients and can exist along with adenopathy in other locations.
Diarrhea: Diarrhea is present in approximately 20% of patients.
Oral ulcers: Ulcers are described in 10-20% of patients.
Neurologic symptoms: These symptoms range from mild to moderate headache in nearly 50% of patients, occasionally severe with meningitis, encephalitis, and/or Guillain-Barre Syndrome.
Opportunistic infections: Although relatively uncommon, some present with oral pharyngeal or esophageal candidiasis or Pneumocystis jiroveci pneumonia.
Laboratory abnormalities: These abnormalities include leukopenia, anemia, thrombocytopenia, and transaminase elevation. During this state of disease, patients can have transient reduction in CD4+ T-cell counts, sometimes below 200 cells/uL. Less common laboratory abnormalities include, but are not limited to, elevation in creatinine, laboratory evidence of rhabdomyolysis, and cerebrospinal fluid pleocytosis.

How did the patient develop acute HIV infection? What was the primary source from which the infection spread?

HIV is primarily transmitted by contact of bodily fluids with mucosal membranes. The likelihood of transmission is directly related to both the volume of fluids a person is exposed to and the level of virus present within the fluids. Bodily fluids that contain significant amounts of infectious HIV are blood, vaginal and seminal fluids, cerebrospinal fluid, and breast milk. The level of HIV present in other bodily fluids, such as sweat, tears, and saliva, is very low.

Sexual exposure

Transmission can occur any time vaginal or seminal fluids come in contact with mucous membranes (e.g., vaginal, anal, or oral mucosa).It is noteworthy that sexual transmission frequently occurs from those unaware of their infection status. Moreover, those with acute infection may contribute disproportionately to transmission events, since these people are engaging in high risk activity, are unaware of their infection status, and tend to have high levels of virus in blood and genital secretions.

Highest risk activity is receptive anal intercourse with lower but significant risk associated with receptive vaginal intercourse, insertive anal and vaginal intercourse, and even lower risk associated with receptive oral sex.
Risk for transmitting to a partner or acquiring infection after sexual exposure is directly related to levels of plasma HIV RNA, which likely correlates with the level of virus present in genital secretions.
Risk of sexual transmission is enhanced in the presence of other genital inflammatory or ulcerative diseases (e.g., vaginitis, urethritis, and herpes simplex infection).
Acquisition of HIV is enhanced in uncircumcised males, compared to those circumcised.
Sexual activity with exposure to blood is likely to be associated with increased risk of HIV transmission.

Blood exposure

The risk of transmission in this setting is directly related to the amount of blood a person is exposed to, the amount of virus present in the blood, and in the setting of needle sticks to the level of penetration into the skin.

Sharing needles for injection of illicit drugs is the most common way HIV is transmitted from exposure to blood.
Sharing needles for injection of other drugs/medications (e.g., use of anabolic steroids) can also transmit HIV.
Exposure to contaminated equipment (e.g., that used for tattooing) transmits HIV.
Sexual activity associated with blood exposure can transmit HIV.
Blood exposure during traumatic events (e.g., an altercation) has been reported.
Occupational exposure in which blood from an infected person penetrates the skin on a sharp object has occurred. Very rarely, transmission has reportedly occurred through contact with breaks in the skin or exposure of mucous membranes (e.g., eyes or mouth) to blood.
Transfusion of blood or blood products has been reported to transmit HIV. In developed countries, the risk of transmission through transfusion is approaching zero.

HIV-infected pregnant or nursing mothers

HIV is efficiently transmitted to newborns during pregnancy and at the time of delivery, as well as from breastfeeding. The risk of transmission is markedly reduced by the mother being placed on effective combination antiretroviral therapy and avoiding breast feeding.

Household contacts

Transmission among household contacts is extremely rare in the absence of sexual exposures or contact with blood. There is a low, but theoretical, risk associated with sharing toothbrushes and razors, both of which can result in blood being exposed to breaks in the skin or mucous membranes. Consequently, these types of household items should not be shared between an HIV-infected and uninfected individual.

Which individuals are at greater risk for developing acute HIV infection?

HIV is sufficiently prevalent in most countries that any exposure to sexual fluids or blood would place someone at risk for acquiring HIV infection. In the past, there was a tendency to consider this diagnosis only in select high risk groups (e.g., drug users and men who have sex with men). Although these groups remain at highest risk, both heterosexual men and women are also at risk. Consequently, although some activities result in greater risk than others, all individuals who have been exposed to bodily fluids should be considered at risk for acute HIV infection and, if presenting with a compatible syndrome, evaluated for this diagnosis.

Beware: there are other diseases that can mimic acute HIV infection:

Although acute HIV infection was originally described as a “mononucleosis-” or “influenza-“ like illness, it can present with a wide variety of clinical and laboratory manifestations, which, based on the findings, can result in a broad differential diagnosis. It should also be noted that the typical tonsillar hypertrophy seen in mononucleosis would be unusual in acute HIV infection. Frequently considered differential diagnoses are:

Pharyngitis: streptococcal infection, Epstein-Barr, cytomegalovirus, toxoplasmosis, or influenza
Oral or genital ulcers: herpes simplex, coxsackie virus, aphthous stomatitis, or Behcet’s disease
Rash: primary herpes simplex, secondary syphilis, enterovirus, rubella, rickettsial diseases, roseola, parvovirus B19, allergic reaction, or rheumatologic disease
Meningitis/encephalitis: enterovirus infection, herpes simplex, West Nile, or other viral encephalitides
Diarrhea: viral or bacterial gastroenteritis
Transaminase elevation: viral hepatitis, cytomegalovirus, Epstein-Barr, or drug reaction

What laboratory studies should you order and what should you expect to find?

The biggest challenge to making the diagnosis of acute HIV infection is thinking of it when a patient presents with any risk factors and a compatible clinical syndrome. This requires abandoning traditional stereotypes as to who is at risk so as to consider the diagnosis in all sexually active individuals and those potentially sharing needles. The second obstacle to making the diagnosis is recognizing that, during this stage of disease, patients are often HIV antibody negative with high levels of circulating virus (see Figure 2). When acute HIV infection is considered in the differential diagnosis, the following tests should be performed:

Timeline for the emergency of viral markers and antibodies during acute HIV infection

Combined screening tests: These tests detect both antibodies against HIV and the p24 antigen. A negative combined screening test is a strong argument against acute HIV infection. In rare cases, HIV-RNA may be present, whereas P24 antigen is still undetectable, so that a repeated combined screening test or a measurement of HIV-RNA may be indicated.

HIV antibody test: If the Western blot is fully positive, the patient has been infected for months to years and it is unlikely that HIV explains the acute symptoms with which the patient presents. If the HIV antibody test is negative or positive with an indeterminate Western blot, the patient may well have acute infection, since, during the first weeks of infection, antibodies are either not present or just starting to emerge. In this case, it is important to either do follow-up antibody testing within the next weeks to verify seroconversion or preferably perform a virologic test.

HIV virologic tests: Unlike the antibody test, which detects the humoral immune response to viral antigens, these tests identify circulating virus in the blood of infected patients. During acute infection, when antibodies are just emerging, the level of virus in blood often exceeds those seen in patients with the most advanced stages of chronic infection. Potential tests include:

p24 antigen: This test is typically positive in those with acute infection while still antibody negative or in the very advanced stages of chronic infection. The sensitivity in those with acute infection without HIV-specific antibodies is approximately 80%, but declines quickly with the emergence of antibodies. The specificity of this test for circulating HIV is greater than 99%. This test can be ordered as an isolated test or as part of a combination assay that detects both HIV antibodies and p24 antigen.
Plasma HIV RNA: This test is routinely used as a quantitative assay in those with chronic infection but has a sensitivity in those with acute infection of approaching 100%. False-positive plasma HIV RNA results can occur; however, this is likely less common with current assays and when it does occur, levels tend to be low (e.g., <5,000 copies/mL). In contrast, those with acute HIV infection and negative antibodies typically have levels greater than 100,000 copies/mL and often in the millions.

Results that confirm the diagnosis of acute HIV infection

The definitive diagnosis of acute HIV infection is made by documenting HIV antibody seroconversion from a negative or indeterminate antibody test to a fully positive Western blot.

A probable and presumptive diagnosis can be made by documenting a positive virologic test in the setting of a negative or indeterminate antibody test or by the combination of a negative screening test in the past and symptoms and signs of acute HIV infection associated with a positive HIV antibody or screening test.

Other situations in which the diagnosis of acute HIV infection is made

There is increasing interest in not missing patients actively seroconverting to HIV. Since signs and symptoms may be absent or minimal, targeted screening of symptomatic patients is likely to miss a substantial number of people. Consequently, approaches have been considered to screen all antibody-negative individuals with a virologic test. In these settings, it is possible that patients will present for routine screening HIV antibody testing and be found seroconverting to HIV. The assays most frequently employed are:

Pooled HIV RNA testing: This involves taking the serum or plasma from those found to be HIV antibody negative on routine screening and pooling them. In this setting, a single HIV RNA assay can determine if HIV is present in any of the pooled samples. Further testing is performed to pinpoint which of the samples included in the pool was actually positive.

HIV antibody/p24 antigen combination assay: This is a standard enzyme-linked immunoassay that detects the presence of HIV antibody, p24 antigen, or both. If the test is positive, the patient can be further evaluated with an HIV antibody test and Western blot, which will define if the reactive result was from the presence of antibodies in a patient with chronic infection versus p24 antigen in an antibody-negative or indeterminate patient.

What is the distinction between "acute" and "early" HIV infection?

Although there are no standardized definitions, in general, the term “acute” refers to the process of seroconverting, often with an acute retroviral syndrome. In contrast, “early” infection refers to those with documented infection in the recent past, usually defined as within the preceding 6 months. Most of the previous discussion focuses on the manifestations and diagnosis of acute HIV infection.

Diagnosis of early infection: Early infection is usually diagnosed in those found to have a positive HIV antibody test after having been documented to be negative within the preceding 6 months. Occasionally, a patient will test positive, believe he or she may have been exposed in the previous few months, and potentially have had a syndrome consistent with acute infection.

In this setting, it is difficult to know whether this is early versus more chronic infection. For epidemiologic studies, there is an interest in identifying these people to enhance the estimates of incident HIV infection. Research assays use a so called “detuned” or “less sensitive” antibody test. When infection has occurred within the previous 6-12 months, the “detuned” assay is negative, whereas the conventional more sensitive screening test is positive. These assays are not commercially available.

Those diagnosed with early infection may or may not have established their virologic and immunologic set-point. In addition, many of the pathogenic events that occur during acute infection have probably already occurred. As with acute infection, the role of treatment during this stage of disease has not been established. Details of the available data are included in the specifics related to the treatment of acute HIV infection.

If you decide the patient has acute HIV infection, what should be done?

All patients diagnosed with HIV infection, and especially those with acute infection, should be referred to someone with expertise in the management of this patient population. The following information should be shared with those with acute HIV infection:

The natural history of HIV disease, emphasizing that this represents the earliest stage of a slowly progressive disease and that most presenting symptoms will resolve with time: This is particularly important since many patients who present with symptomatic acute HIV infection equate their symptoms to those of full blown AIDS.
It should be explained to the patient that he or she was likely infected in the preceding months and that anyone they have exposed to sexual fluids or blood should be notified that they may be infected or at risk for HIV infection as well.
Patients should be counseled regarding how the transmission of HIV and other pathogens can be avoided in the future (e.g., avoid blood exposure, needle sharing, or sex without barrier protection).
Patients should be informed that acute HIV infection represents a unique stage of disease, one in which there remains controversy as to whether antiretroviral therapy should be initiated. A detailed discussion should occur as to the potential rationale for antiretroviral therapy and specific treatment options, ranging from deferring treatment with follow-up of plasma HIV RNA and CD4+ T-cells levels or the early initiation of therapy.
Genotypic drug resistance testing should be performed to determine whether the patient acquired a drug resistant strain of HIV.
Patients should be referred for continuity care that includes further discussion regarding ways to avoid transmission of HIV and other pathogens, as well as health maintenance recommendations. The latter would include healthy lifestyle changes, such as weight loss, exercise, diet, avoiding illicit drug use, and excessive alcohol intake. All patients should be referred to mental health specialists if indicated and be screened for latent tuberculosis, chronic hepatitis B and/or C infection, syphilis, chlamydia/gonorrhea in urine, cervix and anal mucosa, and gonorrhea in oral mucosa. Finally, immunizations should be provided per standard guidelines.

Antiretroviral Treatment of Acute HIV Infection

To quote from the current Treatment Recommendations as published by the NIH in 2016:

Antiretroviral therapy (ART) is recommended for all HIV-infected individuals, regardless of CD4 T lymphocyte cell count, to reduce the morbidity and mortality associated with HIV infection (AI).
ART is also recommended for HIV-infected individuals to prevent HIV transmission (AI).
When initiating ART, it is important to educate patients regarding the benefits and considerations regarding ART, and to address strategies to optimize adherence. On a case-by-case basis, ART may be deferred because of clinical and/or psychosocial factors, but therapy should be initiated as soon as possible.

These recommendations also apply to patients with acute HIV infection. Prevention of transmission is a important concern; such patients are particularly infective because of their high viral load.

The rationale for considering early treatment includes:

Shorten the duration and/or severity of symptoms
Reduce risk for more rapid disease progression
Reduce the risk of transmission to others Preserve immune reserve and gastrointestinal integrity
Preserve HIV-specific immune responses, which might allow for enhanced viral control if treatment is stopped or to be stimulated by therapeutic immunogens that might become available in the future
Limit size of the viral reservoir
Decrease the rate of viral evolution and degree of heterogeneity

Rationale for initiating antiretroviral therapy during acute HIV infection.

There are several reasons given for considering the early initiation of antiretroviral therapy during acute HIV infection. Some might also apply to those with documented “early” infection (e.g., within the preceding 6 months).

To shorten the duration and/or severity of symptoms

Anecdotal evidence indicates that symptoms of the acute retroviral syndrome abate rapidly after starting antiretroviral therapy. However, no controlled studies are available.

To reduce the risk for more rapid disease progression

The data is extremely variable, but there are increasing numbers of retrospective, observational studies that demonstrate a relationship between the number and severity of symptoms associated with acute HIV infection and a variety of measures of disease progression.

If true, it is not clear that starting treatment within days or weeks of acute infection will influence outcome, but it does suggest that patients with symptomatic acute HIV infection are more likely to progress to the point of needing antiretroviral therapy sooner than those with less symptomatic acute infection.

To reduce the risk of transmission to others

The fact that people with acute infection have, by definition, recently been putting themselves and others at risk for HIV infection suggests that every effort needs made to influence the likelihood of transmitting. This would include making the diagnosis and counseling them about safe practices. Indeed, there is data showing that risk taking activity declines in those recently diagnosed with HIV infection, but it is not a consistent effect and often transient.

There is strong biologic data suggesting that people with acute HIV infection are likely to have a greater risk of transmitting to others after single exposures. This is primarily based on the observations that the very high levels of HIV in plasma correlated with levels in genital secretions, both of which are likely to increase transmissibility after isolated exposure to blood or sexual secretions.

Molecular studies demonstrate that people with acute infection may be disproportionately contributing to new cases of infection within a given community. In fact, several studies report up to 30% of incident HIV infections may be from those with acute HIV infection.

The HPTN 052 study demonstrated that, among chronically HIV-infected individuals, the early initiation of antiretroviral therapy reduced the risk of transmission to their seronegative partner by approximately 96%.

To preserve immune reserve and gastrointestinal integrity

There are now several studies demonstrating in both simian immunodeficiency virus models and in humans that, during the first days and weeks of HIV infection, there is a modest decline in peripheral blood CD4+ T-cells with a dramatic decline in gastrointestinal CD4+ T-cells, perhaps more than an 80% loss in this compartment.

Recent studies suggest that the pathogenicity of HIV is not restricted to immune suppression. HIV causes chronic inflammation, which, in turn, may contribute to a variety of diseases in the neurologic, cardiovascular, renal, and hepatic systems. In fact, some of this inflammation and activation persists even in those on antiretroviral therapy with suppressed plasma HIV RNA. It has been hypothesized that this ongoing inflammation may relate to bacterial translocation across an immunologically impaired gastrointestinal tract with increased levels of bacterial products (e.g., lipopolysaccharide in HIV-infected on and off antiretroviral therapy compared to uninfected controls). It is conceivable that therapy during acute infection may be an opportunity to limit the early damage to gastrointestinal lymphoid compartment.

Most data suggests that the initiation of antiretroviral therapy during chronic infection has limited effect on reconstituting gastrointestinal lymphoid compartment. Although even more limited, at this time, it is not clear that initiation of therapy during acute infection would have a greater effect on preserving the immunologic integrity of this compartment or that any differences in the timing of therapy influences the level of bacterial translocation or persistent inflammation and activation.

To preserve HIV-specific immune responses that might allow for enhanced viral control if treatment is stopped or to be stimulated by therapeutic immunogens that might become available in the future

Previous studies demonstrate that those with chronic HIV infection often lack robust HIV-specific immune responses often present in select patients with slow disease progression (e.g., long-term nonprogressors).

It has been hypothesized and reported in select cohorts that treatment during acute HIV infection can protect HIV-specific CD4+ T-cells from HIV infection and destruction, resulting in those treated early having levels of these responses approaching those of long-term non progressors.

Early non-controlled studies reported that those treated during acute HIV infection who had persistently detectable HIV-specific CD4+ T-cells were able to at least transiently demonstrate enhanced virologic control after stopping therapy. Consequently, one reason for considering early therapy in those identified with acute and possibly even early HIV infection was to preserve immune responses so they could discontinue treatment with delayed progression and need for initiation of chronic, long-long antiretroviral therapy.

Three relatively large randomized controlled trials have formally tested this hypothesis by assigning patients identified with acute and/or early HIV infection to either be monitored off antiretroviral therapy or to start treatment for some finite period of time followed by treatment discontinuation and follow-up, which have included the time to meeting criteria for starting antiretrovirals during chronic HIV infection, as well as virologic set-point off treatment. These studies suggest treatment during early and possibly acute infection for 24-48 weeks, but not 12 weeks, may translate into modest benefits regarding time to meeting current guidelines for initiation of antiretroviral therapy and virologic/immunologic setpoints. The benefits are relatively modest and of unclear clinical relevance in an era when guidelines are recommending earlier initiation of therapy because of concerns that ongoing viral replication adversely affects a variety of end organs.

The three recent studies include:

A5217: This study randomized those infected within the preceding 6 months, excluding those with acute infection, to either be monitored off treatment or be treated for 36 weeks and then be monitored off therapy. Key endpoints were the need to start antiretrovirals and viral set-point. This study enrolled approximately 120 patients but was prematurely stopped by an independent Data Safety Monitoring Board because of the high rate of requiring treatment initiation among those randomized to the deferred treatment arm. Overall, there was a significantly lower risk of requiring initiation of therapy among those treated early, but the durability of this effect was not completely defined. Similarly, there appeared to be a difference in the virologic set-point among favoring those that started and then discontinued treatment, but differences were modest.
Primo-SHM Trial: This study randomized those identified with acute or early HIV infection to no treatment versus antiretrovirals for 24 or 60 weeks followed by treatment discontinuation. The study enrolled approximately 120 patients with endpoints including time to requiring initiation of therapy and virologic and immunologic setpoints. Those treated for either 24 or 36 weeks appeared to achieve better outcomes for each endpoint compared to those who did not start treatment, although the differences were relatively modest, including a delay in the time to initiation of therapy being limited to approximately 1-2 years.
SPARTAC Trial: This study randomized 372 individuals with acute or early HIV infection to no treatment versus 12 or 48 weeks of treatment followed by therapeutic interruption with follow-up. The primary endpoint was time to CD4+ T-cell count of less than 350 cells/uL or initiation of treatment. There was a significantly lower risk of needing to initiate therapy in those treated for 48 weeks than those who did not start therapy or were treated for 12 weeks, but this delay was not statistically different from 48 weeks. It is unlikely that SPARTAC will resolve the controversy about indications for treatment one way or another.

To limit size of the viral reservoir

There is clear evidence that the viral reservoir, most often measured as persistently infected resting memory CD4+ T-cells in those on suppressive antiretroviral therapy, is established within days of infection and probably prior to the development of humoral immune responses and the onset of the acute retroviral syndrome.

The clinical relevance of the size of the viral reservoir in treated patients is unknown, but it is generally considered one obstacle to either the long-term control of HIV or eradication from the body.

Data is limited, but some studies suggest that this reservoir may be lower in those treated during acute and even early HIV infection than those treated with chronic infection. Nevertheless, the clinical relevance of these findings at this time is unknown.

To decrease the rate of viral evolution and degree of heterogeneity, and the size of the proviral reservoir

There are many studies showing that those newly infected acquire a relatively homogenous population of HIV that then evolves quickly in vivo.

There are several studies suggesting that the degree of viral heterogeneity is associated with disease progression.

The early initiation of therapy during acute HIV infection will almost certainly limit early viral evolution resulting in reservoirs with relatively homogenous viral population. Although an intriguing rationale for early therapy, the clinical relevance of this early restriction of viral evolution is not known.

Which treatment options should be considered?

There is currently no data suggesting that those treated during acute HIV infection should be offered different antiretroviral therapy options than those with chronic infection. The following issues should be considered:

If there is no evidence of genotypic drug resistant virus present, any of the preferred treatment options for antiretroviral naive patients could be considered (e.g., dual nucleoside reverse transcriptase inhibitors (NRTIs) with a non-nucleoside reverse transcriptase inhibitor (NNRTI), a ritonavir-boosted protease inhibitor (PI/r), or an integrase strand transfer inhibitor (INSTI)).
If genotypic drug resistance is present, this should be considered in treatment decisions, ultimately selecting a regimen that includes three fully active agents.
If therapy is started prior to the availability of drug resistance testing, consideration should be given to initiating a dual NRTI plus PI/r-based regimen, since transmitted resistance to PIs is relatively infrequent and resistance to these drugs is less likely to occur if NRTI resistance is unknowingly present than what would be seen with NNRTI or possibly with an INSTI-containing regimens.

If antiretroviral therapy is initiated during acute HIV infection, how long should treatment be continued?

It is currently recommended that those initiating antiretroviral therapy for chronic HIV infection should remain on some form of treatment indefinitely, unless there is a compelling reason to stop. Treatment during acute and possibly early infection had previously been considered differently for several reasons.

These people are starting treatment much earlier than most and perhaps prior to it being necessary.
Therapy is initiated before it is established how well the person is going to control virus on their own.
One rationale for early treatment is to preserve HIV-specific immune responses that could enhance virologic control once therapy is discontinued (see discussion under rationale for early initiation of therapy).

A French group (Sáez-Cirión A, et al. 2013) has described a series of patients treated during acute or early HIV infection who stopped treatment years later. Contrary to expectations, an estimated 5-15% of these patients did not exhibit the typical rebound of viremia, but remained aviremic. Statistically, this result correlated with a low proviral load. Unfortunately, these correlations were not strong enough to allow individual predictions.

Current considerations with regards to stopping therapy in those treated during acute HIV infection include:

There is emerging data demonstrating that stopping therapy in those with chronic infection are at increased risk of progression of both HIV disease and development of renal, cardiovascular, and hepatic event. How this applies to those starting during acute HIV infection is not known.
Antiretroviral therapy results in declines in markers of inflammation and coagulation, effects lost when therapy is discontinued. This may adversely affect endothelial function and other end organs, perhaps explaining observations.
Thus far, reported clinical trials suggest that those who start therapy during acute and early infection, versus those who do not, have relatively modest delays in the need to start therapy, differences that are relatively small in the context of what will ultimately be life-long therapy.
Those who stop therapy are at some risk of developing an acute retroviral-like syndrome, albeit transient and of unknown long-term clinical relevance.

No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.

Jump to Section