One third of all HIV patients worldwide live in regions where leishmaniasis is endemic (1). Visceral leishmaniasis (VL) caused by the parasite L.donovani is endemic to Bihar, a populous state of 110 million people in East India, which carries an estimated 40% of the world’s VL burden(2). Although Bihar has a relatively low prevalence of HIV (between 0.22 - 0.33%), its high population density means that in absolute numbers an estimated 300,000 people in the state live with HIV/AIDS(3).

Moreover, Bihar is one of the few states in India where the rate of new HIV infections is increasing(4). This has major implications for VL co-infection: like other opportunistic infections in HIV patients, Leishmania amastigotes have evolved strategies to survive (5) which are enhanced by HIV co-infection (6) and accelerate progression of disease(7). This may help explain why the risk of developing VL is estimated to be between 100 and 2300 times higher in HIV-infected individuals than in those who are HIV-negative(8). Evidence on the prevalence of HIV-VL co-infection in India is scarce, although estimates range from 2-6%(9–15). HIV-VL co-infection therefore appears to be an emerging public health issue in India.

There is even less data on comparative characteristics of coinfected patients(9). A recent retrospective observational study described an overall prevalence of HIV in patients ≥14 years old presenting with VL at 5.6%, however within certain age groups it was considerably higher. Of male patients 35 to <45 years old presenting with VL, 5% were unknowingly HIV positive and, when pooled with data on the numbers of already-diagnosed HIV-positive patients presenting with VL, altogether 12.8% and 6.1% of all 35-to <45-year-old men and women, respectively, were co-infected (14).

Yet the evidence base regarding best treatment practices for co-infected patients worldwide is limited, due to a lack of randomized trials and to the fact that most available data comes from observational studies with relatively short follow-up periods, and often with high rates of loss to follow-up(16). Nevertheless, worse outcomes in almost every respect have consistently been reported in this patient group when compared to patients not known to be HIV-positive—for example, in terms of higher relapse rates, mortality, and VL drug toxicity and treatment failure(16).

Following this, an expert committee comprising the respective vertical programmes of the National Vector Born Disease Control Programme (NVBDCP) and National AIDS Control Organisation (NACO) was convened which recommended mandatory HIV testing for all patients diagnosed with VL. However, due to an absence of evidence, no clear recommendations were made on how to effectively screen HIV patients living in VL endemic areas.

There have been a limited number of longitudinal studies frim Bihar and West Bengal to establish the prevalence of exposure and progression of asymptomatic VL patients to symptomatic VL in non-HIV infected patients.  These suggest that asymptomatic VL is 4-17 times more prevalent than symptomatic VL (19). A recent review of these studies estimated the risk of progression from asymptomatic to symptomatic to be between 1.5-23%, being higher in those with high antibody titres (20).  In particular, a recent study from West Bengal suggested that 10.4% of 79 asymptomatic cases testing positive with rk39 progressed to symptomatic VL within 3 years (21).

However there remains no evidence available on the burden of asymptomatic VL cases or pattern and risk factors for progression of asymptomatic cases into to symptomatic VL among people living with HIV (PLHIV) AIDS.  This is a large evidence gap, since VL is considered as an opportunistic infection in HIV, and the GoI has mandated that it be treated as a stage 4 AIDS defining illness. As such, it is highly likely (although not demonstrated) that in KA endemic areas, the prevalence of exposure to VL in HIV patients will be high, and the progression to symptomatic VL much higher than in non-immunocompromised populations. Crucially, unlike non-immunocompromised patients, those presenting with co-infection with HIV and VL currently do so at a very late stage, when treatment outcomes are poor and mortality rates high.

Asymptomatic leishmaniasis are likely to be drivers of VL epidemic and an important challenge to sustain VL elimination(22). Considering the high infectivity, recurring relapses and difficulty in treating co-infected patients, their identification, risk factor stratification for visceralisation and early management needs to be evaluated. This study will fill this knowledge gap, and may lead to further research on lower-dose early treatment of HIV positive asymptomatic infections.