Zhijun Hou

Ticks represent one of the most medically important groups of arthropod vectors worldwide, posing substantial threats to both public health and livestock production through the transmission of vari...

Natural selection is expected to maintain a stable 1:1 sex ratio in randomly mating populations. However, obligate parasites, especially nematodes with complex host-migratory life cycles, often show pronounced departures from this equilibrium. Ascaris suum , a globally distributed nematode with an XX/XO sex-determination system, exhibits an obvious female-biased sex ratio in adults, making it an ideal model to investigate when and how sex-ratio bias arises. Progress has been limited because, at present, no practicable method exists to identify worm sex at stages other than adulthood. Here, we aimed to establish a valid approach designed to be applicable, in principle, for precise sex identification and sex-ratio estimation across all stages of A. suum. Using a chromosome-level A. suum genome assembled in our laboratory (CNP0003380), we identified single-copy sequences on autosomes and the X chromosome and selected 3C (Chr3) as an autosomal marker and 5X (Chr5X) as an X-linked marker. We developed a qPCR assay that infers sex or sex ratio from the 3C/5X copy-number ratio, with theoretical values of 1 for XX females and 2 for XO males. Validation with 30 adult females and 30 adult males yielded 3C/5X ratios of 1.009 ± 0.042 and 1.995 ± 0.054, respectively, with no significant deviation from theoretical expectations ( p > 0.05). The relative abundance of X-bearing to O-bearing sperm measured by qPCR was 0.980 ± 0.093, compared with 1.081 ± 0.163 by flow cytometry. Although the mean values differed significantly between the two methods (paired Students t -test, t = −2.886, d.f. = 29, p = 0.0073), the qPCR-based estimates showed lower variability than those obtained by flow cytometry. These results indicate that this qPCR assay provides an accurate tool for sex identification and quantification of the relative abundance of X-bearing to O-bearing sperm in A. suum.

Enterocytozoon bieneusi is an important zoonotic pathogen. This study examined its prevalence and genotypes in Siberian tigers in Northeast China. Fecal samples from 97 captive and 5 wild tigers were analyzed by nested PCR targeting the ITS region. Prevalence in captive tigers was 40.2% (39/97), with no significant site differences. Three genotypes were identified: D (89.7%), Peru8 (7.7%), and Type IV (2.6%), all within zoonotic Group 1. E. bieneusi was detected for the first time in a wild Siberian tiger (genotype D). The predominance of genotype D—common in poultry—suggests dietary transmission through contaminated chicken meat. These results indicate high prevalence of zoonotic genotypes in tigers, underscoring cross-species transmission risks and the need for strengthened biosecurity and surveillance.

Ticks (Acari: Ixodida) are arachnids classified within the superfamily Ixodoidea and currently divided into four families: Ixodidae (hard ticks), Argasidae (soft ticks), Nuttalliellidae, and Deinoc...

The Alongshan virus (ALSV), a newly identified tick-borne segmented flavivirus, can infect humans and cause Alongshan fever, making it imperative to understand its pathogenic mechanisms for the development of effective intervention strategies. Our previous research has established that ALSV exhibits sensitivity to interferon-beta (IFN-β) while having evolved the ability to antagonize downstream antiviral responses induced by type I IFN (IFN-I); however, the specific effects and underlying mechanisms by which ALSV modulates IFN-I production remain poorly understood. In the present study, we demonstrated that ALSV infection significantly suppresses host IFN-I production triggered by poly(I:C), a synthetic analog of viral double-stranded RNA that activates innate immune pathways. To unravel the molecular basis of this suppression, we systematically evaluated the impact of individual ALSV viral proteins on Toll-like receptor-mediated IFN-I production, revealing a complex regulatory network wherein distinct viral proteins target specific signaling molecules: specifically, VP2 and VP3 were found to be responsible for inhibiting RIG-I-mediated IFN-I production, while NSP2 and VP1b were identified as key inhibitors of MDA5-mediated IFN-I production, highlighting the virus’s strategy of employing multiple proteins to disrupt innate immune signaling. Focusing further on the viral nucleoprotein VP2, we determined that it acts at the upstream signaling level of TANK-binding kinase 1, a critical kinase in the IFN-I signaling cascade. Mechanistically, VP2 directly interacts with RIG-I and mediates its degradation through an autophagy-dependent pathway, thereby impairing the host’s ability to detect viral RNA and initiate IFN-I production. These findings not only expand our understanding of the immune evasion mechanisms employed by novel segmented flaviviruses but also offer valuable insights that could facilitate the development of new preventive and therapeutic strategies for the ALSV infection. IMPORTANCE: Alongshan virus (ALSV) is an emerging segmented flavivirus that poses a growing threat to human and animal health across Eurasia. Despite its demonstrated capacity to infect humans and suppress interferon (IFN)-mediated antiviral responses, the precise mechanisms of ALSV immune evasion remain largely undefined. This study identifies the viral nucleoprotein VP2 as a key antagonist of host type I IFN (IFN-I) production. By directly interacting with and promoting the autophagy-mediated degradation of RIG-I, VP2 effectively disrupts innate immune recognition and signaling. This finding not only elucidates a previously unknown mechanism of immune suppression by ALSV but also highlights the virus’s sophisticated strategy of using multiple proteins to selectively target RIG-I and MDA5 pathways. These insights advance our understanding of segmented flavivirus-host interactions and suggest that restoring RIG-I function may be a promising therapeutic strategy against ALSV infection.

Toxoplasmosis and tick-borne encephalitis (TBE) are endemic in Heilongjiang province, China, posing a significant threat to public health. Although some research has indicated that Toxoplasma gondii infection may suppress the host’s immune response and increase susceptibility to other pathogens, no studies have been conducted to explore the association between these two diseases. From 2020 to 2023, a total of 415 serum samples were collected and tested for both T. gondii and tick-borne encephalitis virus (TBEV) infections using enzyme-linked immunosorbent assay (ELISA) by us. The positive rates of T. gondii and tick-borne encephalitis virus were 14.15% (60/415) and 36.14% (150/415), respectively. The positive rate of tick-borne encephalitis virus was 66.67% (40/60) in T. gondii-positive patients, while it was 30.99% (110/355) in the group of T. gondii-negative patients. A statistically significant correlation was observed between T. gondii infection and the tick-borne encephalitis virus (TBEV) positive status (P < 0.05). Age and occupation were significantly associated with seropositivity of T. gondii (P < 0.05). This finding provides the first indication that individuals infected with T. gondii are more susceptible to tick-borne encephalitis virus (TBEV).

Immunocompromised patients with prolonged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections may serve as reservoirs for viral evolution, with suboptimal immune responses facilitating the accumulation of adaptive mutations. This study aimed to characterize the drivers of SARS-CoV-2 adaptive evolution in such hosts through genomic surveillance. We retrospectively analyzed 24 patients with long-term positive nasopharyngeal reverse transcription-polymerase chain reaction results (symptom onset duration: 7–14 days on average, 1 HIV-positive patient with >20 days of infection). Most infections (April–May 2022) were caused by Omicron variants (predominantly BA.2). Phylogenetic analysis revealed accelerated viral evolution in patients with diverse underlying diseases (e.g., HIV and esophageal cancer). A total of 78 intrahost single-nucleotide variants were identified, with ORF1ab (53.8%) and the Spike protein coding region (20.5%) being hotspots. Notably, the HIV-positive patient’s virus developed unique mutations: NSP3-T779I, NSP15-A94T, and Spike double mutations N440K and I794T. Functional assays showed that the N440K/I794T double mutation significantly enhanced infectivity in Hela-hACE2 cells ( P < 0.05) but reduced immune evasion (50% neutralizing titer increased ~2-fold vs BA.2, P < 0.001). The I794T mutation was later detected in the JN.1.16 strain, suggesting potential evolutionary persistence. Prolonged SARS-CoV-2 replication in immunocompromised hosts, particularly HIV-positive individuals, drives adaptive mutations with altered infectivity and immune evasion. These findings emphasize the need for monitoring such hosts to prevent the spread of potentially transmissible variants. IMPORTANCE: This study reveals the characteristics of adaptive mutations and their biological functions of SARS-CoV-2 during long-term infection in immunocompromised patients, emphasizes the importance of close monitoring of the long-term replication of SARS-CoV-2, aiming to timely detect and prevent the spread of newly emerging neutralization-resistant variants in susceptible populations, and provides a key scientific basis for formulating effective public health prevention and control strategies.