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The heterogeneous nuclear ribonucleoprotein (hnRNP A2B1) is a key component of the hnRNP complex involving RNA modulation in eukaryotic cells and it has also been reported to be involved in the replication of the hepatitis E virus, influenza A virus, and hepatitis B virus. However, it is not clear whether the role of the hnRNP A2B1 in viral replication is conserved among RNA viruses and what is the mechanism of hnRNP A2B1 in RNA virus replication. In this study, we first used severe fever with thrombocytopenia syndrome virus (SFTSV), a tick-borne RNA virus that causes a severe viral hemorrhagic fever as well as other RNA viruses including VSV-GFP, SeV, EV71, and ZIKV to demonstrate that knockout hnRNPA2B1 gene inhibited viral RNA replication and overexpression of hnRNP A2B1 could restore the RNA levels of all tested RNA viruses. These results suggest that hnRNPA2B1 upregulation of viral replication is conserved among RNA viruses. Next, we demonstrated that hnRNP A2B1 was translocated from the nucleus to the cytoplasm under RNA virus infection including SFTSV, VSV-GFP, SeV, EV71, and ZIKV, suggesting translocation of hnRNP A2B1 from the nucleus to the cytoplasm is crucial for RNA virus replication. We then used SFTSV as a model to demonstrate the mechanism of hnRNP A2B1 in the promotion of RNA virus replication. We found that overexpression of SFTSV nucleoprotein can also cause hnRNP A2B1 translocation from the nucleus to the cytoplasm and that the SFTSV NP interacted with the RNA recognition motif 1 domain of hnRNP A2B1. We further demonstrated that the hnRNP A2B1 interacted with the 5' UTR of SFTSV RNA. In conclusion, we revealed that the hnRNP A2B1 upregulation of viral RNA replication is conserved among RNA viruses; the mechanism of hnRNP A2B1 in promotion of SFTSV viral RNA replication is that SFTSV NP interacted with the hnRNPA2B1 to retain it in the cytoplasm where the hnRNP A2B1 interacted with the 5' UTR of SFTSV RNA to promote the viral RNA replication.IMPORTANCESevere fever with thrombocytopenia syndrome virus (SFTSV) is a tick-borne RNA virus with a high mortality rate of up to 30%. In this study, we first used SFTSV as a model to demonstrate that the role of hnRNPA2B1 in viral replication is conserved in SFTSV. Then we used other RNA viruses, including VSV-GFP, SeV, EV71, and ZIKV, to repeat the experiment and demonstrated the same results as SFTSV in all tested RNA viruses. By knocking out the hnRNPA2B1 gene, SFTSV RNA replication was inhibited, and overexpression of hnRNPA2B1 restored RNA levels of SFTSV and other tested RNA viruses. We revealed a novel mechanism where the SFTSV nucleoprotein interacts with hnRNPA2B1, retaining it in the cytoplasm. This interaction promotes viral RNA replication by binding to the 5' UTR of SFTSV RNA. The findings suggest that targeting hnRNPA2B1 could be a potential strategy for developing broad-spectrum antiviral therapies, given its conserved role across different RNA viruses. This research provides significant insights into the replication mechanisms of RNA viruses and highlights potential targets for antiviral interventions.
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Severe fever with thrombocytopenia syndrome is an emerging viral hemorrhagic fever caused by a tick-borne bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV), with a high case fatality. We previously found that SFTSV nucleoprotein (NP) induces macroautophagy/autophagy to facilitate virus replication. However, the role of NP in antagonizing host innate immunity remains unclear. Mitophagy, a selected form of autophagy, eliminates damaged mitochondria to maintain mitochondrial homeostasis. Here, we demonstrate that SFTSV NP triggers mitophagy to degrade MAVS (mitochondrial antiviral signaling protein), thereby blocking MAVS-mediated antiviral signaling to escape the host immune response. Mechanistically, SFTSV NP translocates to mitochondria by interacting with TUFM (Tu translation elongation factor, mitochondrial), and mediates mitochondrial sequestration into phagophores through interacting with LC3, thus inducing mitophagy. Notably, the N-terminal LC3-interacting region (LIR) motif of NP is essential for mitophagy induction. Collectively, our results demonstrated that SFTSV NP serves as a novel virulence factor, inducing TUFM-mediated mitophagy to degrade MAVS and evade the host immune response.
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Phenuiviruses are a class of segmented negative-sense single-stranded RNA viruses, typically consisting of three RNA segments that encode four distinct proteins. The emergence of pathogenic phenuivirus strains, such as Rift Valley fever phlebovirus (RVFV) in sub-Saharan Africa, Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) in East and Southeast Asia, and Heartland Virus (HRTV) in the United States has presented considerable challenges to global public health in recent years. The innate immune system plays a crucial role as the initial defense mechanism of the host against invading pathogens. In addition to continued research aimed at elucidating the epidemiological characteristics of phenuivirus, significant advancements have been made in investigating its viral virulence factors (glycoprotein, non-structural protein, and nucleoprotein) and potential host-pathogen interactions. Specifically, efforts have focused on understanding mechanisms of viral immune evasion, viral assembly and egress, and host immune networks involving immune cells, programmed cell death, inflammation, nucleic acid receptors, etc. Furthermore, a plethora of technological advancements, including metagenomics, metabolomics, single-cell transcriptomics, proteomics, gene editing, monoclonal antibodies, and vaccines, have been utilized to further our understanding of phenuivirus pathogenesis and host immune responses. Hence, this review aims to provide a comprehensive overview of the current understanding of the mechanisms of host recognition, viral immune evasion, and potential therapeutic approaches during human pathogenic phenuivirus infections focusing particularly on RVFV and SFTSV.
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Interacciones Huésped-Patógeno , Inmunidad Innata , Humanos , Interacciones Huésped-Patógeno/inmunología , Phlebovirus/inmunología , Phlebovirus/genética , Phlebovirus/patogenicidad , Evasión Inmune , Factores de Virulencia/genética , Factores de Virulencia/inmunología , Virus de la Fiebre del Valle del Rift/inmunología , Virus de la Fiebre del Valle del Rift/genética , Virus de la Fiebre del Valle del Rift/patogenicidad , Sistema Inmunológico/virología , Sistema Inmunológico/inmunologíaRESUMEN
Anaplasma and Ehrlichia are tick-borne bacterial pathogens that cause anaplasmoses and ehrlichioses in humans and animals. In this study, we examined the prevalence of Anaplasma and Ehrlichia species in ticks and domesticated animals in Suizhou County, Hubei Province in the central China. We used PCR amplification and DNA sequencing of the 16S rRNA, groEL, and gltA genes to analyze. We collected 1900 ticks, including 1981 Haemaphysalis longicornis and 9 Rhipicephalus microplus, 159 blood samples of goats (n = 152), cattle (n = 4), and dogs (n = 3) from May to August of 2023. PCR products demonstrated that Anaplasma bovis, Anaplasma capra, and an Ehrlichia species were detected in the H. longicornis with the minimum infection rates (MIR) of 1.11%, 1.32%, and 0.05%, respectively; A. bovis, A. capra, and unnamed Anaplasma sp. were detected in goats with an infection rate of 26.31%, 1.31% and 1.97%, respectively. Anaplasma and Ehrlichia species were not detected from cattle, dogs and R. microplus ticks. The genetic differences in the groEL gene sequences of the Anaplasma in the current study were large, whereas the 16S rRNA and gltA gene sequences were less disparate. This study shows that ticks and goats in Suizhou County, Hubei Province carry multiple Anaplasma species and an Ehrlichia species, with relatively higher infection rate of A. bovis in goats. Our study indicates that multiple Anaplasma and Ehrlichia species exist in ticks and goats in the central China with potential to cause human infection.
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Anaplasma , Anaplasmosis , Animales Domésticos , Ehrlichia , Variación Genética , Cabras , ARN Ribosómico 16S , Animales , Anaplasma/genética , Anaplasma/aislamiento & purificación , China/epidemiología , Ehrlichia/genética , Ehrlichia/aislamiento & purificación , Cabras/microbiología , Perros , Bovinos , Anaplasmosis/epidemiología , Anaplasmosis/microbiología , Prevalencia , Animales Domésticos/microbiología , ARN Ribosómico 16S/genética , Garrapatas/microbiología , Ehrlichiosis/epidemiología , Ehrlichiosis/veterinaria , Ehrlichiosis/microbiología , FilogeniaRESUMEN
Cyclic GMP-AMP synthase (cGAS) is an important DNA pattern recognition receptor that senses double-stranded DNA derived from invading pathogens or self DNA in cytoplasm, leading to an antiviral interferon response. A tick-borne Bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV), is an RNA virus that causes a severe emerging viral hemorrhagic fever in Asia with a high case fatality rate of up to 30%. However, it is unclear whether cGAS interacts with SFTSV infection. In this study, we found that SFTSV infection upregulated cGAS RNA transcription and protein expression, indicating that cGAS is an important innate immune response against SFTSV infection. The mechanism of cGAS recognizing SFTSV is by cGAS interacting with misplaced mitochondrial DNA in the cytoplasm. Depletion of mitochondrial DNA significantly inhibited cGAS activation under SFTSV infection. Strikingly, we found that SFTSV nucleoprotein (N) induced cGAS degradation in a dose-dependent manner. Mechanically, N interacted with the 161-382 domain of cGAS and linked the cGAS to LC3. The cGAS-N-LC3 trimer was targeted to N-induced autophagy, and the cGAS was degraded in autolysosome. Taken together, our study discovered a novel antagonistic mechanism of RNA viruses, SFTSV is able to suppress the cGAS-dependent antiviral innate immune responses through N-hijacking cGAS into N-induced autophagy. Our results indicated that SFTSV N is an important virulence factor of SFTSV in mediating host antiviral immune responses. IMPORTANCE: Severe fever with thrombocytopenia syndrome virus (SFTSV) is a tick-borne RNA virus that is widespread in East and Southeast Asian countries with a high fatality rate of up to 30%. Up to now, many cytoplasmic pattern recognition receptors, such as RIG-I, MDA5, and SAFA, have been reported to recognize SFTSV genomic RNA and trigger interferon-dependent antiviral responses. However, current knowledge is not clear whether SFTSV can be recognized by DNA sensor cyclic GMP-AMP synthase (cGAS). Our study demonstrated that cGAS could recognize SFTSV infection via ectopic mitochondrial DNA, and the activated cGAS-stimulator of interferon genes signaling pathway could significantly inhibit SFTSV replication. Importantly, we further uncovered a novel mechanism of SFTSV to inhibit innate immune responses by the degradation of cGAS. cGAS was degraded in N-induced autophagy. Collectively, this study illustrated a novel virulence factor of SFTSV to suppress innate immune responses through autophagy-dependent cGAS degradation.
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Inmunidad Innata , Nucleoproteínas , Nucleotidiltransferasas , Phlebovirus , Phlebovirus/genética , Phlebovirus/inmunología , Nucleotidiltransferasas/metabolismo , Nucleotidiltransferasas/genética , Humanos , Nucleoproteínas/metabolismo , Nucleoproteínas/genética , Nucleoproteínas/inmunología , Células HEK293 , Síndrome de Trombocitopenia Febril Grave/virología , Síndrome de Trombocitopenia Febril Grave/inmunología , Síndrome de Trombocitopenia Febril Grave/metabolismo , Autofagia , Animales , ADN Mitocondrial/genética , ADN Mitocondrial/metabolismo , Interferones/metabolismo , Interferones/inmunología , Interferones/genética , Proteínas Virales/metabolismo , Proteínas Virales/genéticaRESUMEN
Severe fever with thrombocytopenia syndrome virus (SFTSV) nonstructural protein (NSs) is an important viral virulence factor that sequesters multiple antiviral proteins into inclusion bodies to escape the antiviral innate immune response. However, the mechanism of the NSs restricting host innate immunity remains largely elusive. Here, we found that the NSs induced complete macroautophagy/autophagy by interacting with the CCD domain of BECN1, thereby promoting the formation of a BECN1-dependent autophagy initiation complex. Importantly, our data showed that the NSs sequestered antiviral proteins such as TBK1 into autophagic vesicles, and therefore promoted the degradation of TBK1 and other antiviral proteins. In addition, the 8A mutant of NSs reduced the induction of BECN1-dependent autophagy flux and degradation of antiviral immune proteins. In conclusion, our results indicated that SFTSV NSs sequesters antiviral proteins into autophagic vesicles for degradation and to escape antiviral immune responses.
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Herpesviruses are large double-stranded DNA viruses that cause infections in animals and humans with a characteristic of latent infectious within specific tissues. Bats are natural hosts of variety human-infecting viruses and recently have been described as hosts for herpesviruses in several countries around the world. In this study we collected 140 insectivorous bats in the neighboring urban areas of Wuhan City, Hubei Province in the central China between 2020 and 2021. Nested PCR targeting the dpol gene sequence indicated that a total of 22 individuals (15.7% of the sample) tested positive for herpesvirus with 4 strains belonging to the genus Betaherpesvirus and the remaining 18 strains classified as Gammahersvirus. Furthermore, the herpesvirus prevalence in Rhinolophus pusillus was higher at 26.3%, compared to 8.4% in Myotis davidii. The RP701 strain from R. pusillus was the predominant gammaherpesvirus strain detected in bats, accounting for 94.4% (17/18) of all strains. The variations in γ-herpesviruses genomic sequences was evident in phylogenetic tree, where RP701 strain was clustered together with ruminant γ-herpesviruses, while MD704 strain formed a distinct clade with a hedgehog γ-herpesvirus. Four betaherpesviruses exclusively identified from M. davidii, with nucleotide identities ranging from 79.7 to 82.6% compared to known betaherpesviruses. Our study provided evidence that M. davidii can sever as natural host for ß-herpesviruses, which extended the host species range. In conclusion, we found that bats from central China harbored novel ß-herpesviruses and γ-herpesviruses which were phylogenetically related to ruminant γ-herpesvirus and hedgehog γ-herpesvirus. Our study indicates that bats are natural hosts of ß- and γ-herpesviruses and further studies are needed to determine whether there is cross-species transmission of herpesviruses between bats and other animals, or humans.
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Betaherpesvirinae , Quirópteros , Gammaherpesvirinae , Infecciones por Herpesviridae , Filogenia , Animales , Quirópteros/virología , China/epidemiología , Gammaherpesvirinae/genética , Gammaherpesvirinae/aislamiento & purificación , Gammaherpesvirinae/clasificación , Betaherpesvirinae/genética , Betaherpesvirinae/aislamiento & purificación , Betaherpesvirinae/clasificación , Infecciones por Herpesviridae/veterinaria , Infecciones por Herpesviridae/virología , Infecciones por Herpesviridae/epidemiología , Genoma Viral , ADN Viral/genéticaRESUMEN
Background: Severe fever with thrombocytopenia syndrome (SFTS) is an emerging hemorrhagic fever caused by a tick-borne bunyavirus SFTSV with case fatality up to 30%. The reactivation of Epstein-Barr virus (EBV) has been proven to occur in individuals with various immune suppression conditions. Methods: Here, we diagnosed 22 SFTSV infected patients with PCR in a hospital in Shandong Province, China in 2020. To understand the consequences of SFTSV infection leading to EBV reactivation, we examined EBV reactivation in SFTSV-infected patients with PCR and RT-PCR. Results: We found that EBV was reactivated in 18.2% (4/22) of SFTS patients, suggesting that EBV reactivation is common in SFTS patients. Compared with SFTS patients without EBV reactivation, SFTS patients with EBV-reactivation had a significantly lower median level of serum albumin (32.45 g/L vs. 26.95 g/L, p = 0.03) and a significantly higher median number of urine red blood cells (0 cells/µL vs. 9 cells/µL, p = 0.04). Conclusion: SFTS infection can reactivate EBV in patients, which may make the clinical condition of patients worsen.
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BACKGROUND: The order Rickettsiales contains a group of vector-borne gram-negative obligate intracellular bacteria, which often cause human emerging infectious diseases and economic losses for dairy and meat industries. The purpose of this study is to investigate the distribution of the pathogens including Rickettsia spp., Anaplasma spp., and Ehrlichia spp. in the order Rickettsiales in ticks from Yueyang, a prefecture-level city of Hunan Province in Sothern China, and assess the potentiality of transovarial transmission of these rickettsial organisms. METHODS: Ticks were collected from cattle in a farm in Yueyang City and the tick DNA was used as template to amplify the htrA, rrs, gltA, ompA and ompB genes of Rickettsia as well as rrs and groEL genes of Anaplasma and Ehrlichia. RESULTS: All ticks (465) collected were the cattle tick, Rhipicephalus microplus. PCR showed the minimum infection rate (MIR) was 1.5% (7/465) for Candidatus Rickettsia xinyangensis, 1.9% (9/465) for C. Anaplasma boleense, 1.3% (6/465) for Anaplasma platys, 0.6% (3/465) for A. marginale, and 1.17% (2/465) for each of A. bovis, Ehrlichia minasensis, and a non-classified Ehrlichia sp. A human pathogen, C. Rickettsia xinyangensis and A. platys were detected in 100% (3/3) and 33.3% (2/6) laboratory-hatched larval pools from infected females respectively. CONCLUSION: Our study revealed a diversity of pathogenic rickettsial species in R. microplus ticks from Hunan Province suggesting a threat to people and animals in China. This study also provided the first molecular evidence for the potential transovarial transmission of C. Rickettsia xinyangensis and A. platys in R. microplus, indicating that R. microplus may act as the host of these two pathogens.
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Escarabajos , Rhipicephalus , Rickettsia , Animales , Femenino , Humanos , Rickettsia/genética , Larva , Ehrlichia/genética , Rickettsiales , Anaplasma/genéticaRESUMEN
Hemoplasmas can cause severe hemolytic anemia in humans. To explore the genetic diversity and the potential transmission routes of hemoplasmas among bat population, bats and bat-ectoparasites including bat-flies, bat-mites, and bat-ticks were collected in Eastern and Central China from 2015 to 2021, and tested with PCR for hemoplasmas 16S rRNA gene. Based on 16S rRNA PCR, 18.0% (103/572) adult bats were positive for hemoplasmas, but none of 11 fetuses from hemoplasmas-positive pregnant bats was positive for hemoplasmas. These results indicated that adult bats had a high prevalence of hemoplasma, but vertical transmission of hemoplasmas did not occurr in the bats. Based on the 16S rRNA gene PCR, the minimum infection rate of bat-ectoparasite for hemoplasmas was 4.0% (27/676), suggesting that bat-ectoparasite also had a high prevalence for hemoplasmas. Phylogenetic analysis revealed that bat hemoplasmas from this study clustered into 4 genotypes (I-IV). Genotype I clustered together with hemoplasmas identified in bats from America. Genotype II shared high similarity with a human-pathogenic hemoplasma Candidatus Mycoplasma haemohominis. Genotype III and IV were unique, representing 2 new hemoplasma genotypes. Only genotype I was identified in both bats and all bat-ectoparasites including bat-flies, bat-mites, and bat-ticks. In conclusion, bats and bat-ectoparasites from China harbored abundant genetically diverse hemoplasmas including potential human-pathogenic hemoplasmas, indicating bats and bat-ectoparasites may play important roles in the maintenance and transmission of hemoplasmas in the natural foci.
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Ticks pose a serious threat to public health as carriers and often vectors of zoonotic pathogens. There are few systematic studies on the prevalence and genetic diversity of tick-borne bacterial pathogens in Western China. In this study, 465 ticks were collected from free-ranging sheep in Gansu Province in China. Ticks were divided into 113 pools and tick DNA was extracted from these ticks. PCR assays were performed using specific primers to screen for tick-borne pathogens as well as sequence analysis based on the 16S rRNA (rrs), ompB, gltA, ompA genes for Rickettsia, rrs, groEL genes for Anaplasma, and ssrA and rpoB genes for Bartonella. The PCR results showed that the minimum infection rates with Rickettsia, Anaplasma, and Bartonella were 16.8% (78/465), 18.9% (88/465), and 0.9% (4/465), respectively. Sequence analysis based on the concatenated sequences of rrs-ompB-gltA-ompA indicated that the Rickettsia species identified in the ticks belonged to Rickettsia raoultii, Rickettsia slovaca, and Rickettsia sibirica, respectively; phylogenetic analysis based on the groEL gene showed that all Anaplasma strains identified were Anaplasma ovis; and phylogenetic analysis based on the ssrA and rpoB genes indicated that all Bartonella strains in the ticks belonged to Bartonella melophagi. The results of this study showed that ticks in Gansu Province harbored multiple pathogens that may cause rickettsial diseases and bartonellosis. These diseases were neglected in the area and physicians and public health workers need to pay attention to their diagnoses to prevent human infection.
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Bartonella , Ixodidae , Rickettsia , Garrapatas , Animales , Ovinos , Humanos , Garrapatas/microbiología , Anaplasma/genética , Filogenia , ARN Ribosómico 16S/genética , Ixodidae/microbiología , Rickettsia/genética , Bartonella/genética , China/epidemiologíaRESUMEN
Severe fever with thrombocytopenia syndrome virus (SFTSV), a tick-borne Bunyavirus, causes an emerging hemorrhagic fever in humans with a high fatality in Asia. The tick vectors and hosts of SFTSV are not well studied. We evaluated SFTSV transmission in laboratory reared Haemaphysalis flava ticks. RT-PCR demonstrated that after acquisition feeding in SFTSV-infected rabbits, 10 % (4/40) engorged larvae, 25% (5/20) engorged nymphs, and 50% (5/10) engorged females of H. flava became SFTSV RNA positive; after engorged larvae and nymphs molted into nymphs and adults, respectively, 12.5% (3/24) newly molted nymphs and 20% (2/10) newly molted adults were SFTSV RNA positive. Among 30 engorged females that oviposited, 10% (3/30) clutches of eggs and 3.3% (1/30) colonies of larvae were RNA positive for SFTSV. RT-PCR also showed that 6 days after being infested with SFTSV-infected ticks, 100% (3/3) rabbits infested with larvae, 100% (2/2) rabbits infested with nymphs, and 100% (2/2) rabbits infested with adult ticks became SFTSV RNA positive. In conclusion, H. flava can acquire SFTSV from infected rabbits by feeding; there is transstadial and transovarial transmission of the virus and all three stages of H. flava can transmit SFTSV to rabbits by feeding. Thus, H. flava tick is an effective vector of SFTSV and may play a role in the transmission of SFTSV in wild animals and humans.
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Ixodidae , Phlebovirus , Síndrome de Trombocitopenia Febril Grave , Garrapatas , Animales , Humanos , Femenino , Conejos , Ixodidae/genética , Phlebovirus/genética , ARNRESUMEN
Vaccines have been considered the most promising solution for ending the coronavirus disease 2019 (COVID-19) pandemic. Information regarding neutralizing antibodies (NAbs) and T-cell immune response in inactivated SARS-CoV-2 vaccine-immunized COVID-19 convalescent patients were either only available for a short time after illness recovered or not available at all (T-cell immunity). We evaluated SARS-CoV-2 NAbs and cellular immune responses to the SARS-CoV-2 inactivated vaccine in convalescent patients who recovered from infection for about one and a half years. We found that compared to before vaccination, SARS-CoV-2 NAbs and specific T-cell responses were significantly boosted by the inactivated vaccine in convalescent patients, which confirmed the pre-existing adaptive immunity in SARS-CoV-2 infected people. We observed that NAbs and IFN-γ-secreting T-cell response elicited by a single vaccine dose in subjects with prior COVID-19 infection were higher than after two doses of vaccine in SARS-CoV-2 naïve subjects. Both humoral and cellular immune responses elicited by one and two doses of inactivated vaccine were comparable in COVID-19-recovered persons. In conclusion, inactivated COVID-19 vaccine induced robust NAbs and T-cell responses to SARS-CoV-2 in COVID-19 convalescent patients and immune responses after one dose were equal to that after receiving two doses, which highlighted that robust humoral and cellular immune response can be reactivated by the inactivated vaccine in SARS-CoV-2 convalescent patients.
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Bartonella are vector-borne gram-negative facultative intracellular bacteria causing emerging infectious diseases worldwide, and two thirds of known Bartonella species are carried by rodents. We captured rodents, shrews and rodent ectoparasitic mites in rural areas of Qingdao City, Shandong Province, China from 2012 to 2021 and used the animal spleen tissues for the PCR amplification of Bartonella gltA and rpoB genes. PCR showed 9.4% (40/425) rodents, and 5.1% (12/235) shrews were positive for Bartonella. Seven Bartonella species including three novel species were identified in five rodent species and one shrew species, indicating the abundance and genetic diversity of Bartonella in rodents and shrews. The infection rate of each Bartonella species in the animal species was as below: novel Candidatus Bartonella crocidura in shrews Crocidura lasiura (5.1%, 12/235); novel Candidatus Bartonella cricetuli in hamsters Tscherskia triton (20%, 9/45); novel Candidatus Bartonella muris in striped field mice Apodemus agrarius (4.2%, 7/168) and house mice Mus musculus (1.5%, 2/135); Bartonella fuyuanensis in striped field mice (8.9%, 15/168) and house mice (0.7%, 1/135); Bartonella rattimassiliensis and Bartonella tribocorum in brown rats Rattus norvegicus (6.7%, 3/45 and 4.2%, 2/45, respectively); Bartonella queenslandensis in Chinese white-bellied rat Niviventer confucianus (12.5%, 1/8). These results suggest that Bartonella infected a variety of rodent and shrew species with high infection rate, but each Bartonella specie is restricted to infect only one or a few genetically closely related rodent species. In addition, Candidatus Bartonella cricetuli, Candidatus Bartonella muris and Bartonella coopersplainsensis were found in chigger Walchia micropelta (33.3%, 3/9), and B. fuyuanensis were found in chigger Leptotrombidium intermedium (4.1%, 1/24), indicating chiggers may be reservoirs of Bartonella. In conclusion, abundant genetic diversified Bartonella species are found to infect rodents, shrews and chiggers, but each Bartonella species has a strict rodent animal host specificity; and chigger mites may play a role in Bartonella transmission.
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Infecciones por Bartonella , Bartonella , Enfermedades de los Roedores , Ratas , Animales , Roedores/microbiología , Musarañas/microbiología , Especificidad del Huésped , Reservorios de Enfermedades/microbiología , Bartonella/genética , Infecciones por Bartonella/epidemiología , Infecciones por Bartonella/veterinaria , Infecciones por Bartonella/microbiología , Murinae , China/epidemiología , Variación Genética , Enfermedades de los Roedores/epidemiología , Enfermedades de los Roedores/microbiologíaRESUMEN
We sequenced DNA from spleens of rodents captured in rural areas of Qingdao, East China, during 2013-2015. We found 1 Apodemus agrarius mouse infected with Rickettsia conorii, indicating a natural Mediterranean spotted fever foci exists in East China and that the range of R. conorii could be expanding.
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Fiebre Botonosa , Ratones , Animales , Fiebre Botonosa/epidemiología , Fiebre Botonosa/microbiología , Roedores , China/epidemiologíaRESUMEN
We report a patient in China with fever of unknown origin who visited 3 hospitals in 3 weeks and was finally given a diagnosis of acute Q fever, determined by metagenomics next-generation sequencing. Our results indicate that physicians are unfamiliar with Q fever and the disease is neglected in China.
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Fiebre Q , Humanos , Fiebre Q/diagnóstico , Diagnóstico Tardío , China/epidemiología , Fiebre/diagnósticoRESUMEN
SFTSV, a tick-borne bunyavirus causing a severe hemorrhagic fever termed as severe fever with thrombocytopenia syndrome (SFTS). To evaluate the potential role of rodents and its ectoparasitic chiggers in the transmission of SFTSV, we collected wild rodents and chiggers on their bodies from a rural area in Qingdao City, Shandong Province, China in September 2020. PCR amplification of the M and L segments of SFTSV showed that 32.3% (10/31) of rodents and 0.2% (1/564) of chiggers (Leptotrombidium deliense) from the rodents were positive to SFTSV. Our results suggested that rodents and chiggers may play an important role in the transmission of SFTSV, although the efficiency of chiggers to transmit SFTSV needs to be further investigated experimentally.
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Infecciones por Bunyaviridae , Infestaciones por Ácaros , Phlebovirus , Garrapatas , Trombiculidae , Animales , China/epidemiología , Fiebre , Phlebovirus/genética , RoedoresRESUMEN
BACKGROUND: As of 2022, inactivated SARS-CoV-2 vaccines had been used in more than 91 countries. However, limited real world information was available on the immune responses of the inactivated SARS-CoV-2 vaccine. METHODS: We used SARS-CoV-2 pseudovirues to determine the neutralizing antibodies (NAbs) to wild type and several global variants and utilized enzyme-linked immunosorbent assay to investigate IFN-γ-secreting T-cell responses to SARS-CoV-2 among 240 vaccinated individuals after two doses of inactivated vaccine in China. RESULTS: A majority of the vaccinated (>90%) developed robust NAbs and T-cell responses to SARS-CoV-2 in the first two months after the second dose. After six months, only 37.0% and 44.0% of vaccinees had NAbs and T-cell immunity to SARS-CoV-2, respectively. Immune serum retained most of its neutralizing potency against the Alpha and Iota variants, but lost significant neutralizing potency against the Beta, Kappa, Delta, and Omicron variants. Only 40% of vaccine-sera retained low-level neutralization activities to Omicron, with a 14.7-fold decrease compared to the wild type. CONCLUSION: The inactivated SARS-CoV-2 vaccine stimulated robust NAbs and T-cell immune responses in the first two months after the second dose but the immune effect dropped rapidly, highlighing that a third dose or additional booster immunizations may be required to boost immunity against SARS-CoV-2.
Asunto(s)
COVID-19 , Vacunas Virales , Anticuerpos Neutralizantes , Anticuerpos Antivirales , COVID-19/prevención & control , Vacunas contra la COVID-19 , Humanos , Sueros Inmunes , Inmunidad Celular , SARS-CoV-2 , Vacunas de Productos InactivadosRESUMEN
Background: The delta variant (B.1.617.2) of SARS-CoV-2 was the dominant viral strain causing COVID-19 in China, 2021. We reported a SARS-CoV-2 delta variant outbreak in Jingmen City, Hubei Province, China. Methods: The data of epidemiological, clinical, laboratorial, and vaccination of COVID-19 cases were collected through field investigation and analyzed. Results: During the outbreak from 4 to 20 August 2021, 58 cases of the SARS-CoV-2 delta variant (B.1.617.2) were identified with 15 (25.9%) asymptomatic and 43 (74.1%) symptomatic (mild and moderate) patients. The mean serial interval was 2.6 days (standard deviation: 2.0, 95% CI: 1.9-3.6). The median age of the patients was 39 years (ranging from 1 to 60 years) with the high proportion in children (19.0%). The secondary attack rate was 9.8% higher from parents to their children (<18 years) (46.2%, 95% CI: 14.8-77.5%) than that between spouses (36.4%, 95% CI: 14.5-58.2%), but no significant difference was observed (p > 0.05). Approximately half (27; 46.6%) of cases were vaccine breakthrough infections. In vaccine breakthrough cases (fully vaccinated), viral loads decreased 1.9-3.4-folds (p < 0.05), duration of viral shedding shortened 5 days (p < 0.05), and the risk of becoming symptomatic from asymptomatic decreased 33% (95% CI: 5-53%) (aged ≥12 years) than those in unvaccinated infections. Conclusions: Children are highly susceptible to the SARS-CoV-2 delta variant in the COVID-19 outbreak in Jingmen City in 2021. Inactivated vaccine derived from wide-type strain can effectively reduce the viral load, duration of viral shedding, and clinical severity in vaccine breakthrough cases. Our study indicates that protective measures that include full vaccination against COVID-19, especially in children, should be strengthened.