Key result
Herpesviridae causes ~4% of CNS infections, predominantly driven by CMV in PLWHA presenting with meningitis.
Why the study?
This study was conducted to describe the clinical and laboratory aspects of central nervous system infections caused by Herpesviridae in a tertiary infectious diseases hospital.
CMV is the most prevalent Herpesviridae causing CNS infections in this cohort, particularly in patients living with HIV/AIDS, and molecular methods are essential for identifying the etiologic agent.
Molecular testing is essential in PLWHA with CNS infection; reinforces CMV predominance among Herpesviridae in immunocompromised cohorts.
The Herpesviridae family includes viruses with latency capacity, such as HSV-1, HSV-2, VZV, CMV, and Human herpesvirus 6, which can cause neurological manifestations such as meningitis, encephalitis, and encephalomyelitis. HSV-1 infection is the prototype of encephalitis, while HSV-2 and VZV are frequent causes of meningitis and meningoencephalitis. CMV mainly affects immunosuppressed patients, such as transplant recipients and people living with HIV/AIDS (PLWHA). This study describes clinical and laboratory aspects of central nervous system (CNS) infections by Herpesviridae between 2017 and 2022 in a tertiary infectious diseases hospital. Descriptive retrospective cohort study based on medical record review. Patients with CNS infection confirmed by multiplex PCR (BioFire FilmArray® Panel) in cerebrospinal fluid, from 2017 to 2022, were included. Of 1,562 patients evaluated, 64 (4%) had confirmed infection by viruses of the Herpesviridae family: HSV-1 (n=4; 6.25%), HSV-2 (n=14; 21.9%), Herpesvirus 6 (n=13; 20.3%), CMV (n=18; 28%), and VZV (n=15; 23.4%). Clinical syndromes were meningitis (n=42; 65.62%), encephalitis (n=17; 26.56%), and meningoencephalitis (n=5; 7.81%). The most frequent encephalitis agent was VZV (n=7; 41.17%), followed by CMV (n=6; 35.29%). In HSV-1 and HSV-2 infections, there was male predominance (ratio 14:5), with a mean age of 39 years. CMV infections showed male predominance, mean age 39 years, and association with HIV/AIDS in 94.4%. CSF showed a mean cell count of 315 cells/mm³ (lymphocytic predominance), mean protein level of 234 mg/dL, and mean glucose level of 55 mg/dL. ADA was assessed in 30 patients (mean 7.3 U/L) and lactate in 2 (mean 10.6 mg/dL). Treatment used was acyclovir (48.4%) for HSV-1, HSV-2, and VZV, and ganciclovir (77.7%) for CMV. Eleven patients had coinfections with other agents: CMV/Human herpesvirus 6/Cryptococcus neoformans/gattii (n=1), CMV/VZV (n=2), VZV/Human herpesvirus 6 (n=2), S. pneumoniae/HSV-2 (n=2), Enterovirus/Human herpesvirus 6 (n=2), HSV-2/Human herpesvirus 6 (n=2). A relevant number of CNS infections caused by Herpesviridae were identified. CMV was more prevalent in PLWHA. CSF in these infections generally shows a lymphomononuclear pattern, without hypoglycorrhachia and with elevated protein, and diagnosis depends on clinical–laboratory correlation. Molecular methods assist in identifying the etiologic agent.
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Farias et al. (2026) studied this question. Among 1,562 patients with CNS infections, 4% had confirmed Herpesviridae infections, predominantly CMV in PLWHA, and clinical syndromes included meningitis (66%).
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