BK and JC polyomaviruses (BKPyV and JCPyV) are widespread among healthy human populations, as approximately 90 % and 80 % of adults present antibodies against BKPyV and JCPyV, respectively [1]. The primary infection is generally asymptomatic and usually takes place during childhood or early adulthood. Transmission occurs through the respiratory route and possibly by the faecal-oral route as well [1]; however, transmission by semen, blood product transfusion, and organ transplantation have also been proposed [2,3].

After primary infection, both viruses can remain latent in many sites, such as the kidney, central nervous system (CNS), and lymphoid cells. Reactivation of the latent infection may take place subsequently in immunocompromised and healthy individuals but is more likely to occur in patients with impaired immune function, e.g., T-cell deficiencies [1].

JCPyV is a polyomavirus well known due to its neurotropism and ability to infect the CNS; thus, in immunocompromised patients, JCPyV is the causative agent of progressive multifocal leukoencephalopathy (PML), a fatal neurological disease that affects around 5 % of patients with HIV/AIDS [4]. It has been suggested that different JCPyV genotypes have variable neurotropic properties [5], being genotype 2 frequently associated with PML [6,7]. Conversely, infection by BKPyV is mainly associated with haemorrhagic cystitis and ureteral stenosis in immunocompromised patients [8]; however, meningoencephalitis caused by BKPyV may lead to a fatal outcome when associated with AIDS [9], and the clinical presentation can be devastating, often resulting in death from multi-organ failure [3].

Thereby, despite neurological diseases caused by polyomavirus in immunocompromised individuals are usually associated with JCPyV infection, the etiological role of BKPyV in these cases is not fully understood. In this sense, BKPyV-DNA has been detected in brain tissue and cerebrospinal fluid (CSF) of both immunocompetent and immunocompromised individuals with and without neurological symptoms [[9], [10], [11], [12]]. Moreover, during the last ten years, increasing evidence that the role of BKPyV in neurological diseases should not be underestimated has been reported [[13], [14], [15], [16], [17], [18], [19]].

Some reports describe BKPyV infection in adult and pediatric-transplanted patients in different provinces of Argentina [[20], [21], [22], [23], [24]]; while other authors report the finding of JCV and BKPyV in river waters and urine samples from subjects infected with HIV-1 [25]. However, there is still scarce knowledge about the role of JCPyV, and nothing is known about the role of BKPyV in neurological diseases of immunocompromised or HIV/AIDS patients in Argentina.

Herein, we describe the first evidence of BKPyV and JCPyV infections in CFS samples from HIV/AIDS patients with meningoencephalitis or PML from Argentina.