Global efforts to eradicate smallpox—an Orthopoxvirus infection—began in the mid-20th century, with the last naturally occurring case reported in 1977. This was achieved through global solidarity efforts that expanded the smallpox eradication vaccination program. Approximately 50 years following the cessation of mass smallpox vaccination and in the absence of access to a sustainable boosting program, the population immunologically naïve to Orthopoxviruses has increased significantly. With increasing global movements and travels, we argue that the emergence of two back-to-back yet distinct mpox epidemics in the 21st century is a sign of humanity’s lost herd immunity to Orthopoxviruses. This needs concerted efforts to restore.

Background: Marburg virus disease (MVD) is a viral hemorrhagic fever caused by species members of the Marburgvirus genera, family Filoviridae. Clinical manifes-tations resemble those of the other generic Viral Hemorrhagic Fevers—like ebola virus disease (EVD). Because of biosafety and bio-risk concerns arising from the highly in-fectious nature of filoviruses, postmortems are generally contra-indicated. Thus, de-scription of gross pathological and histopathological findings remains poor. Here, we describe the autopsy findings following a rare co-incidental post-mortem done on a 30 male patient, later confirmed to have MVD. Results: (a) External examination revealed body of a male adult in good nutritional state and no external injuries; (b) Internal examination showed mild ascites in the peritoneal cavity with marked pallor of internal organs. The stomach and intestines were filled with blood without any focal organic lesions. There were petechial hem-orrhages in the sub-pleura of both lungs, but no focal lesions in lungs. The other organs had no gross lesions; (c) Microscopic examination of lung, kidney and liver detailed marked intra-alveolar hemorrhages, tubular necrosis in the kidneys and extensive necrosis in the liver with foci of thrombi in major vessels; (d) a diagnosis of massive hemorrhage and disseminated intravascular coagulation (DIC) was made; and immediate cause of death attributed to hemorrhagic shock. Conclusions: MVD is associated with intra-luminal GIT hemorrhage and DIC in major organs (lungs, kidneys, & liver) resulting in focal or extensive necrosis. Malaria co-infection, in absence of early specific biomarkers may have delayed the suspicion for a VHF in this patient. To enhance early detection of VHFs, there is a need for early biomarkers of VHFs.

Efforts towards an effective HIV-1 vaccine have remained mainly unsuccessful. There is increasing evidence for a potential role of HLA-C-restricted CD8+ T cell responses in HIV-1 control, including our recent report of HLA-C*03:02 among African children. However, there are no documented optimal HIV-1 CD8+ T cell epitopes restricted by HLA-C*03:02; additionally, the structural influence of HLA-C*03:02 on epitope binding is undetermined. Immunoinformatics approaches provide a fast and inexpensive method to discover HLA-restricted epitopes. Here, we employed immunopeptidomics to identify HLA-C*03:02-restricted CD8+ T cell epitopes. We identified a clade-specific Gag-derived GY9 (GTEELRSLY) HIV-1 p17 matrix epitope exclusively restricted to HLA-C*03:02. Residues E62, T142, and E151 in the HLA-C*03:02 binding groove and positions p3, p6, and p9 on the GY9 epitope are crucial in shaping and stabilizing the epitope binding. Our findings support the growing evidence of the contribution of HLA-C molecules to HIV-1 control and provide a prospect for vaccine strategies.

In May 2026, the Democratic Republic of the Congo declared an outbreak of Bundibugyo virus disease (BVD) caused by Bundibugyo ebolavirus (BDBV), for which no licensed vaccine or antiviral treatment was available. We analysed the epidemic trajectory through 14 July 2026 and developed conditional six-month projections. Aggregated data from official INSP/COUSP Situation Reports (14 May–14 July 2026), supplemented by WHO and UN reports, were used to describe cases, deaths, case-fatality ratios (CFRs), and geographic spread. Log-linear models estimated phase-specific growth rates and doubling times; logistic, Gompertz, and constant-incidence scenarios were used for projections, with model comparison, Bayesian sensitivity analysis, deterministic sensitivity bounds, CFR confidence intervals, and rolling-origin validation. Confirmed cases increased from 8 to 2,073, with 796 deaths (national CFR, 38.4%), while affected health zones increased from 3 to 45 across five provinces. Doubling time increased from 8.9 to 19.5 and 25.1 days, representing a 64.1% reduction in growth rate. Ituri accounted for 89.9% of cases, while North Kivu had a CFR of 58.7%. Six-month projections ranged from 2,624 cases under rapid containment to 3,942 under continued deceleration and 10,839 with persistent recent incidence. Although proportional growth slowed, transmission and geographic expansion remained active. The divergence between modelling approaches and systematic under-prediction in temporal validation indicate substantial forecast uncertainty; projections should therefore be interpreted as conditional planning scenarios rather than deterministic forecasts.