Background: An imbalance in the rumen microbiota caused by high-concentrate diets (HCD) is a significant endogenous trigger of mastitis. However, the underlying mechanisms remain largely unknown. Microbial extracellular vesicles (mEVs) are critical mediators of microbe-host communication. However, the role of mEVs in rumen microbiota-mediated mastitis has not yet been reported. In this study, we used an HCD-induced rumen microbiota dysbiosis model to investigate the role of mEVs-derived from rumen microbiota in the pathogenesis of mastitis.
Results: Our results indicate that HCD leads to mastitis and systemic inflammation. Meanwhile, HCD-fed goats exhibited substantial rumen microbiota dysbiosis and the disruption of the rumen barrier. Transplanting rumen microbiota from HCD goats into mice induced both mastitis and systemic inflammation in the recipients. Specifically, HCD increases the production of mEVs carrying microbial DNA, which can translocate across the compromised rumen barrier to the mammary gland, triggering a mammary inflammatory response via activation of the cGAS-STING-NF-κB/NLRP3 pathway. Furthermore, treating mice with mEVs isolated from the rumen fluid of HCD goats directly induced mastitis, whereas depletion of microbial DNA attenuated mEVs-induced mastitis.
Conclusion: Our findings suggest that HCD induces rumen microbiota dysbiosis and impairs rumen barrier function. This dysfunction leads to an increase in microbial DNA-containing mEVs, which subsequently leak into the mammary gland. Once there, these mEVs activate the cGAS-STING-NF-κB/NLRP3 signaling pathway, ultimately inducing mastitis. This study provides a new perspective on the "rumen microbiota-mammary gland axis" and enhances the understanding of the pathogenesis of mastitis.
Viral infections of the ocular surface significantly contribute to morbidity and visual impairment globally. The herpes simplex virus (HSV), adenovirus, cytomegalovirus (CMV), and human papillomavirus (HPV) are predominant pathogens impacting the cornea and conjunctiva, resulting in recurrent illness, epidemic outbreaks, and virus-associated neoplasia. Progress in virology, immunology, and molecular diagnostics has enhanced comprehension of host-virus interactions and introduced novel therapeutic opportunities. A narrative literature review was performed utilizing PubMed, Scopus, and Web of Science, encompassing papers published from 2000 to 2025, with a specific focus on research from 2020 onwards. Eligible publications were peer-reviewed clinical and experimental investigations, together with reviews that focused on epidemiology, etiology, diagnostic methodologies, and therapeutic alternatives. Research indicates that HSV keratitis is the predominant infectious cause of corneal blindness in high-income nations, although adenovirus persists in instigating epidemics of keratoconjunctivitis in the absence of licensed antiviral treatments. CMV keratitis, previously confined to immunocompromised persons, is now acknowledged in immunocompetent patients as a causative agent of corneal endotheliitis. HPV is associated with ocular surface squamous neoplasia, especially in areas with elevated ultraviolet exposure and high human immunodeficiency virus prevalence. Innovative molecular diagnostics, innovative antiviral agents, immunomodulatory approaches, and immunization initiatives signify significant progress that could enhance preventative and therapeutic results.
Background: Cytomegalovirus (CMV) reactivation is a potentially severe complication in immunocompromised patients, yet its incidence and impact in recipients of autologous hematopoietic stem cell transplantation (AHSCT) remain insufficiently documented.
Aim: To assess the frequency, timing, and outcomes of CMV reactivation in patients undergoing AHSCT at Aziza Othmana Hospital.
Methods: We conducted a retrospective descriptive study of all patients who underwent AHSCT between January 2022 and December 2024 and had at least one post-transplant plasma viral load (VL) assessment. CMV VL was quantified by real-time polymerase chain reaction using TaqMan probes (GeneProof®) with a sensitivity threshold of 150 IU/mL.
Results: Among 277 AHSCT recipients, 17 (6.1%) experienced CMV reactivation. Their median age was 43 years, with a sex ratio of 0.46 (male/female). Underlying diseases included large B-cell lymphoma (n = 5), multiple myeloma (n = 3), and Hodgkin's lymphoma (n = 4). The median time to reactivation was 26 days post-transplant (11 days after neutrophil recovery). Median peak VL was 1325 IU/mL (range: 150-641000 IU/mL). Six patients required antiviral therapy (median peak VL: 30150 IU/mL), while 11 had spontaneous resolution (median peak VL: 1320 IU/mL). Two patients died in the context of CMV reactivation.
Conclusion: CMV reactivation occurs in a noteworthy proportion of AHSCT recipients and may lead to severe outcomes. Routine VL monitoring in the early post-transplant period is crucial, and preemptive therapy should be initiated once clinically relevant VL thresholds are reached to prevent progression to CMV disease and associated mortality.
Background: Human immunodeficiency virus (HIV) recency testing provides data that can be used to monitor the trend of new HIV infections. The effectiveness of using people identified with recent infection to identify partners with new HIV infection through partner notification services (PNS) is not well documented.
Aim: To determine the pooled prevalence of recency testing coverage, recent infection, reclassification (recent to long-term infection) and PNS cascade among newly diagnosed people living with HIV.
Methods: PubMed, Cochrane Library and Embase were searched for articles published between January 2018 and November 2024. Studies were included if they reported recency coverage and/or PNS among people newly diagnosed with HIV and used recent infection testing algorithm (RITA). Recency coverage was defined as proportion of people tested using rapid testing for recent infection (RTRI) among those newly diagnosed with HIV. RITA further classifies RTRI results using viral load results (≥ 1000 copies/mL vs < 1000 copies/mL) to confirm recency status. For studies with PNS, we evaluated the cascade: Number of partners elicited, successfully contacted, eligible for HIV testing, tested and HIV diagnosis. PNS effectiveness was measured by proportion of new HIV diagnoses from tested partners. Using random effects models, we computed the pooled estimate of recency outcomes and 95% confidence intervals (CIs).
Results: Twenty-five studies from 17-low- and middle-income countries were included. Of 276315 newly diagnosed people living with HIV, 79864 underwent RTRI with an overall pooled recency coverage of 87% (95%CI: 67-96). The pooled prevalence of RTRI and RITA recency were 12% (95%CI: 9-16) and 7% (95%CI: 4-10), respectively. Pooled prevalence of RTRI reclassification was 34% (95%CI: 22-49). Of the recent cases who agreed to PNS, 253 partners were elicited with an estimated elicitation ratio of 1:1.6. Among partners elicited, 99% were successfully contacted, 75% were eligible for testing, 68% tested for HIV, and 15% were diagnosed with HIV.
Conclusion: High recency testing coverage among newly diagnosed individuals demonstrates the feasibility of monitoring new HIV infections in LMIC. While PNS yielded moderate HIV diagnoses, its targeted approach remains a critical strategy for identifying undiagnosed cases.
Hepatitis A virus (HAV) infection remains a significant public health concern in many developing countries. The annual incidence of HAV infection is 1.5 million, though this figure may be underestimated owing to the infection's asymptomatic nature and the presence of milder disease variants. The clinical spectrum of HAV infection now ranges from asymptomatic infection to fulminant hepatitis. Despite the availability of safe and highly effective vaccines, HAV infections remain a major contributor to acute viral hepatitis worldwide.

