I have always urged patients not to delay HIV testing, especially in Singapore where HIV tests, HIV PEP (Post Exposure Prophylaxis) and various clinical resources are abundantly available.
Some are reluctant to undergo testing because of fear, denial, anxiety, or mere unawareness. The reasons for delaying HIV testing can be more complicated than it seem,[1] and might even differ between various demographics.
Singer Michael Stipe from the famous rock band R.E.M. lamented,
“I was afraid to get tested for HIV for fear of quarantine, the threat of internment camps and having my basic civil rights stripped away. I waited five years to get my first anonymous test. I am happy that attitudes have matured and changed.”
No matter what the reasons or misconceptions are for delayed HIV testing, there exist important scientific bases for early testing.
In order to better understand why early testing and diagnosis are paramount, we can begin with basic HIV microbiology.
What happens after a high-risk exposure to HIV?
There is a period of Acute (Primary) HIV Infection that occurs 1 to 4 weeks after viral transmission via HIV exposure. This period of infection is accompanied by a burst of viral replication and a concurrent decline in CD4 cell count. Most patients manifest a flu-like or mononucleosis-like syndrome, which is frequently missed.
This is subsequently followed by seroconversion with the development of a positive HIV antibody test, usually within 4 weeks of the Acute HIV Infection, and definitely by 6 months after exposure.
Early diagnosis of HIV infection allows several important clinical decisions to be made during this acute phase.
There is now evidence that therapy for Acute (Primary) HIV Infection has its benefits. Although no prospective clinical studies have conclusively demonstrated the benefits, two randomized and one observational study strongly suggest benefits of early therapy.[2]
For example, the SPARTAC Trial Investigators have shown that a 48-week course of antiretroviral therapy (ART) taken in the early stages of HIV infection slows the damage to the immune system, and also delays the need for long-term treatment.[3]
This study is in fact the largest clinical trial ever undertaken that investigates treatment of patients with recent HIV infection. SPARTAC (Short Pulse Anti-Retroviral Therapy at HIV Seroconversion), a randomized controlled trial involving 366 adults over a period of 5 years, was funded by the Wellcome Trust and coordinated by researchers from Imperial College London and the Medical Research Council’s Clinical Trials Unit. The University of Oxford also participated in its immunology research.
Several observational studies have already suggested that treatment during Acute HIV Infection could delay the amount and speed of immune damage, and thus delaying the need to start lifelong antiretroviral medications. SPARTAC is the first large randomized study to test this hypothesis.
The SPARTAC researchers found that on average, subjects who had received no medication needed to begin taking a lifelong course of antiretroviral therapy (ART) 157 weeks after infection.
However, those subjects who received antiretroviral medications for 48 weeks took an average of 222 weeks before beginning long-term antiretroviral therapy (ART). This delay of 65 weeks represents an important delay compared with the no treatment group.
Moreover, participants on the 48-week course of medications had higher CD4 T-cell counts than those in the other treatment groups. This potentially reduces their risk of developing opportunistic, secondary infections. They also had lower levels of HIV RNA in their blood (lower virologic “set point”) for more than a year after stopping treatment compared to the other treatment groups. This could mean reduction in the risk of passing on the virus to sexual partners.
In summary, the benefits of treatment of Acute HIV Infection include the hastening of symptoms resolution, reduction of viral “set point,” lowering the risk of viral transmission to sexual partners, reduction of viral reservoir in the body, and the preservation of CD4 T-cell responses.
Besides allowing the initiation of treatment of early HIV infection, early diagnosis of HIV enables early testing of HIV Resistance Genotype. This early testing of transmitted HIV viral drug resistance to antiretroviral therapy is important for the management of HIV infection. Transmitted drug resistance is more easily detectable during Acute HIV Infection than chronic disease. Antiretroviral therapy (ART) can be started pending the results of the test.
Unless regularly tested, most patients will not be aware that they are HIV positive in the first few years after they have become infected. Early HIV symptoms can be similar to those of influenza or other viral infections, and for most patients, there follows an asymptomatic period of several years when they carry the HIV virus but are not feeling sick.
Early HIV testing is advised if you have been exposed to the virus. Furthermore, regular testing is recommended if your lifestyle puts you at high risk for HIV infection.
Yes, it’s better late than never. But you’ll be far better off early than late.
Do discuss with your doctor concerning rapid HIV tests, HIV RNA PCR tests, HIV P24 antigen / antibody Combo or Duo testing, or HIV PEP if you have been exposed here in sunny Singapore.
Footnotes
[1] “Delayed testers often ultimately tested because of an illness, cited fear as a reason for not testing, identified themselves as low risk, and were non-disclosing of their HIV-seropositive status. Overall, our findings suggest that delayed testers tend to be marginalized, less sexually active with male partners, and non-disclosive about their sexual practices, as well as less likely to recognize their HIV acquisition risks and less likely to express a responsibility to themselves or others to disclose their HIV status.” Cf. Why the Wait? Delayed HIV Diagnosis among Men Who Have Sex with Men. J Urban Health Jul 2010; 87(4):642-655
[2] N Engl J Med 2013; 368:207-217; N Engl J Med 2013; 368:218; J Infect Dis. 2012 Jan 1;205(1):87.
[3] N Engl J Med 2013; 368:207-217
