Hepatitis C Virus (HCV) co-infection and its genotypic distribution in people living with Human Immunodeficiency Virus (HIV) show global inconsistency. Therefore, the present study aimed to investigate the prevalence and genotypic distribution patterns of HCV, along with viral load, in people living with HIV. This cross-sectional study was conducted at SRL Diagnostics Nepal, Pvt. Ltd. in 203 HIV-seropositive patients attending the Tribhuvan University Teaching Hospital (TUTH), Maharajgunj, Kathmandu, Nepal from October 2021 to May 2022. The viral load and HCV genotypes were estimated from RNA extracted from the blood sample (plasma) of PLHIV by using a standard Q-PCR protocol. HCV infection was considered as a core variable, whereas covariates used for this study were duration of HIV infection, age, sex, and ART regimen. Out of total 203 PLHIV, the estimated prevalence of HCV co-infection was 115 (56.6%). Male gender was a unique characteristic associated with a high prevalence of HCV co-infection compared to females. The HCV viral load among PLHIV ranged from 34 to 3,000,000 IU/mL. Among HCV co-infected PLHIV, 56 (48.69%) had a low level of HCV viral load. Interestingly, only 3 (2.6%) patients had an HCV viral load higher than 3,000,000 IU/mL. Diverse HCV genotypes were found in the population, including genotypes 1, 1a, 3a, 5a, and 6. However, genotype 3 was the most prevalent HCV variant among HCV-co-infected PLHIV, with a distribution of 36 (61.1%) and viral load ranging from 34 to 3000 IU/mL. HCV co-infection is frequent in the Nepalese population of people living with HIV, particularly due to HCV genotypic variant 3. The findings of this study could be useful for the management and clearance of the HCV co-infection in PLHIV, aiming to provide a good quality of life.

The maxillary sinus is frequently implicated in facial pain syndromes arising from infection, neoplasia, dental procedures, and, importantly, migraine, which can mimic “sinus headache” and contribute to misdiagnosis and inappropriate antibiotic use. Despite the clinical burden of chronic maxillary sinus pain, the sensory neuron subtypes that convey nociceptive and mechanosensory signals from the sinus mucosa remain incompletely defined. In this study, trigeminal ganglion (TG) neurons innervating the maxillary sinus (sinus TG neurons) were retrogradely labeled with DiD in mice and characterized using ex vivo patch-clamp electrophysiology and single-cell RT-PCR. Sinus TG neurons were found to be predominantly small-diameter, C-afferent nociceptors with electrophysiologic features including high thresholds, repetitive firing, and broad action potentials. Notably, sinus TG neurons formed a distinct molecular and functional subgroup: they expressed Nav1.9, while showing minimal Nav1.8 expression and limited overlap with Nav1.8-positive nociceptor populations. A majority of sinus TG neurons were mechanically responsive, generating mechanically activated currents with heterogeneous adaptation profiles, and a subset expressed the mechanoreceptor Piezo2. Collectively, these findings identify sinus TG neurons as a specialized population of Nav1.9-enriched C-afferent nociceptors with mechanosensitive properties, providing a mechanistic framework for pressure-evoked sinus pain. This work advances the neurobiological basis of sinus-related pain and suggests that Nav1.9 and mechanoreceptor pathways may be potential therapeutic targets for conditions in which sinus symptoms overlap with migraine and other craniofacial pain disorders.

The maxillary sinus is frequently implicated in facial pain syndromes arising from infection, neoplasia, dental procedures, and, importantly, migraine, which can mimic “sinus headache” and contribute to misdiagnosis and inappropriate antibiotic use. Despite the clinical burden of chronic maxillary sinus pain, the sensory neuron subtypes that convey nociceptive and mechanosensory signals from the sinus mucosa remain incompletely defined. In this study, trigeminal ganglion (TG) neurons innervating the maxillary sinus (maxillary sinus TG neurons) were retrogradely labeled with the fluorescent dye DiD in mice and characterized using ex vivo patch-clamp electrophysiology and single-cell RT-PCR. Maxillary sinus TG neurons were found to be predominantly small-diameter, C-afferent nociceptors with electrophysiologic features including high thresholds, repetitive firing, and broad action potentials. Notably, maxillary sinus TG neurons formed a distinct molecular and functional subgroup: they expressed Nav1.9, while showing minimal Nav1.8 expression and limited overlap with Nav1.8-positive nociceptor populations. A majority of maxillary sinus TG neurons were mechanically responsive, generating mechanically activated currents with heterogeneous adaptation profiles, and a subset expressed the mechanoreceptor Piezo2. Collectively, these findings identify maxillary sinus TG neurons as a specialized population of Nav1.9-enriched C-afferent nociceptors with mechanosensitive properties, providing a mechanistic framework for pressure-evoked sinus pain. This work advances the neurobiological basis of sinus-related pain and suggests that Nav1.9 and mechanoreceptor pathways may be potential therapeutic targets for conditions in which sinus symptoms overlap with migraine and other craniofacial pain disorders.