Viral infection is a significant cause of morbidity and mortality following allogeneic hematopoietic stem cell transplantation (Allo-HSCT), largely due to its impact on and interaction with immune reconstitution. Both innate and adaptive immunity are essential for effective viral control, yet their recovery post-transplant is often delayed or functionally impaired. Emerging evidence suggests genetic variation, particularly polymorphisms in the IL28B gene (encoding IFN-λ3), as a critical factor influencing the quality and timing of immune responses during the early post-transplant period. This review explores the role of IL28B polymorphisms in shaping antiviral immunity, in general, as well as after Allo-HSCT. IL28B variants have been implicated in modulating interferon-stimulated gene (ISG) expression, natural killer (NK) cell activity, and type I/III interferon signaling, all central components of innate immune defense against viral infections. Furthermore, IL28B polymorphisms, particularly rs12979860, have been shown in both general populations and limited HSCT cohorts to alter T cell response and interferon production, affecting reactivation and clearance of multiple viruses such as cytomegalovirus (CMV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein–Barr virus (EBV), COVID-19, and BK polyomavirus (BKPyV) as well as Graft vs. Host disease, thereby affecting adaptive immune reconstitution and long-term viral control. Understanding how IL28B genotype alters immune dynamics in transplant recipients could enhance risk stratification for CMV and other diseases and inform personalized prophylactic or therapeutic strategies. Therefore, this review highlights IL28B as a promising biomarker and potential immunoregulatory target in the management of viral infection post-Allo-HSCT.

Chronic obstructive pulmonary disease (COPD) is a well-known respiratory illness. COPD patients oscillate between a stable state and an exacerbated state that leads to disease deterioration. Studies suggest that respiratory microbiome dysbiosis plays a vital role in COPD pathogenesis. However, the exact microbial composition among different clinical states of COPD is still elusive. To determine and compare the respiratory microbiota composition in different COPD clinical states, namely, the stable state (S-COPD) and the acute exacerbated state (AE-COPD). In this prospective study, 74 samples were collected from COPD patients. The sputum microbiota was analyzed via 16 S rRNA gene sequencing, and only 35 samples were included due to bad reads or not in accordance with inclusion criteria: S-COPD patients ( n = 18), and AE-COPD patients ( n = 17). Bioinformatics analysis was used to determine changes in the microbiota among the comparison groups. The most abundant phyla among all the samples were Proteobacteria, Fusobacteria, Firmicutes, and Actinobacteria, with Paracoccus , Streptomyces Leptotrichia Fusobacterium and Ruminococcaceae being the most prevalent genera. Dissimilarity in abundance across the studied COPD states was observed, with significantly greater abundance of Proteobacteria and Fusobacteria in S-COPD patients and greater abundance of Firmicutes in AE-COPD patients at the phylum level. At the genus level, Paracoccus , Fusobacterium , Streptococcus , Haemophilus , and Moraxella were significantly different between the two groups and were more prevalent in S-COPD, whereas Cellulosilyticum , Streptomyces , Leptotrichia , Ruminococcaceae_UCG_014 , and Atopobium were more prevalent in exacerbated individuals. Alpha diversity revealed greater diversity in stable versus exacerbated patients, and a PCoA plot of Bray‒Curtis and weighted UniFrac distances revealed that stable patients were highly clustered, whereas exacerbated patients were more disseminated. At the genus level, LEfSe analysis revealed the dominance of Cellulosilytic , Liptotrichia , and Streptomyces in the AE-COPD group, whereas the S-COPD group microbiome was dominated by the genera Paracoccus , Fusobacterium , Streptococcus Haemophilus , and Moraxella ( p < 0.05). The results of the present study suggest that COPD patients have unique microbial profiles that differ across different states, with increased abundances of Proteobacteria, chiefly Paracoccus . These findings need more research to clarify the definite role of microbiome dysbiosis in COPD pathogenesis.