Background: Pneumonia has a high incidence rate and is a major cause of mortality in children, mostly community-acquired pneumonia (CAP). Human bocavirus (HBoV), since it first identified in 2005, has been repeatedly associated with respiratory tract infections. Nevertheless, the role and related information of HBoV as a pathogen of CAP has not been fulfilled. Here our study is to assess the epidemiological and clinical features in HBoV-positive children with CAP. Methods: A total of 878 secretions of lower respiratory samples were obtained, multiplex PCR was used to detect HBoV and other respiratory viruses. Results: Of all cases, HBoV was detected in 10.0%, with a peak incidence of infection among children < 2 year old, and predominantly noted in autumn and winter. Only 8 patients were HBoV single infection. Co-infection with other respiratory viruses was observed in 86.4%. Moreover, co-infection with bacteria occurred in 27.3% and with Mycoplasma pneumoniae (MP) in 33.0% of HBoV-positive patients. Among all HBoV-positive samples co-infected with bacteria, 87.5% are gram negative bacteria. Compared with HBoV-negative group, age (P = 0.048), wheezing (P = 0.015), tachypnea (P = 0.016), lactate dehydrogenase (P = 0.026) and severe pneumonia (P = 0.023) were statistically significant in HBoV-positive patients. Furthermore, HBoV-positive patients less than 1 year old were more likely to have co-infection with bacteria (P = 0.007). Conclusions: HBoV can be detected alone in respiratory samples of children with CAP, maybe it is one of the causes of CAP in infants. The high incidence of severe pneumonia was found in HBoV-positive patients compared with HBoV-negative cases may indicate a relationship between severe pneumonia and HBoV.

Minute virus of canines (MVC) is an autonomous canine parvovirus that causes severe pathological outcomes, including embryo mortality, spontaneous abortion, and congenital malformations in neonatal puppies. Although MVC infection has been shown to induce host cell cycle arrest and apoptosis, the underlying regulatory mechanisms that coordinate cell proliferation and control apoptotic responses during viral replication remain poorly understood. Sirtuin 1 (SIRT1) is an NAD⁺-dependent deacetylase that plays a critical role in regulating cell cycle progression, DNA damage responses, and apoptosis. However, its involvement in MVC infection has not been fully elucidated. Herein, we show that MVC infection markedly upregulates the mRNA and protein expression levels of SIRT1 in a time-dependent manner. MVC infection activates the SIRT1-p53 signaling axis and modulates the acetylation status of p53. In addition, MVC alters the subcellular distribution of SIRT1, promoting its nuclear translocation and colocalization with the viral protein VP2. Functional analyses demonstrated that pharmacological activation of SIRT1 enhanced the viability of MVC-infected WRD cells (virus-tropic cell), promoting viral replication, prolonging S-phase arrest, and reducing apoptosis. Conversely, inhibition of SIRT1 produced the opposite effects, which were closely associated with regulation of the SIRT1-p53 signaling axis. Moreover, SIRT1 knockdown accelerated apoptosis and attenuated S-phase arrest, whereas SIRT1 overexpression further strengthened S-phase retention. Collectively, our findings identify the SIRT1-p53 signaling axis as an important regulator of cell cycle progression and apoptosis during MVC infection, highlighting SIRT1 as a key host factor that supports viral replication and persistence and a potential target for antiviral intervention.

Objective To analyze the characteristics of lung microbiota in patients with invasive pulmonary aspergillosis (IPA) and see if the microbiome can predict how IPA will turn out. Methods A retrospective analysis was conducted on 189 hospitalized patients with invasive pulmonary aspergillosis (IPA) and patients with other lung infections hospitalized at Ningxia Medical University General Hospital, using propensity score matching. By analyzing the upper and lower respiratory tract microbial specimens from both groups, the composition and diversity differences of lung microbiota were evaluated, as well as their predictive ability for clinical outcomes in IPA patients. Results The airway microbiota of IPA patients showed a notable increase in bacterial diversity; the Firmicutes phylum and the Acinetobacter and Pseudomonas genera might raise the risk of developing IPA. The bacterial diversity in the lung microbiota failed to predict clinical outcomes. Conclusion Unlike previous studies that reported a significant loss of bacterial diversity in the respiratory tracts of IPA patients, this study found that IPA patients actually had more bacterial diversity in their airways. Specific phyla and genera may increase the risk of IPA, but bacterial diversity doesn't really help predict how patients will do. This shows that the changes in lung microbiota over time may promote the onset of IPA and further alter the lung microbiota.