Herpes simplex virus (HSV), including HSV-1 and HSV-2, is an important pathogen that can cause many diseases. Usually these diseases are recurrent and incurable. After lytic infection on the surface of peripheral mucosa, HSV can enter sensory neurons and establish latent infection during which viral replication ceases. Moreover, latent virus can re-enter the replication cycle by reactivation and return to peripheral tissues to start recurrent infection. This ability to escape host immune surveillance during latent infection and to spread during reactivation is a viral survival strategy and the fundamental reason why no drug can completely eradicate the virus at present. Although there are many studies on latency and reactivation of HSV, and much progress has been made, many specific mechanisms of the process remain obscure or even controversial due to the complexity of this process and the limitations of research models. This paper reviews the major results of research on HSV latency and reactivation, and discusses future research directions in this field.
Herpes Simplex ; virology ; Herpesvirus 1, Human ; physiology ; Humans ; Virus Activation ; physiology ; Virus Latency ; physiology ; Virus Replication

Hepatitis B virus ; drug effects ; physiology ; Hodgkin Disease ; drug therapy ; Humans ; Immunoconjugates ; therapeutic use ; Virus Activation ; drug effects

Although vestibular neuritis is defined as acute peripheral vestibulopathy without associated hearing loss, a handful of cases reported sudden hearing loss without concurrent vertigo during follow-up of vestibular neuritis. In addition, some patients show benign paroxysmal postional vertigo(BPPV) ipsilateral to the lesion side with various interval after vestibular neuritis, and they are considered to be "secondary" BPPV. Viral and vascular etiologies have been assumed for the vestibular neuritis but, both of those failed to explain exact pathomechanism so far. Authors experienced a case of sudden hearing loss with simultaneous ipsilateral BPPV after vestibular neuritis. There has been no report of concurrent of BPPV and sudden hearing loss after vestibular neuritis. Sequential viral activations are considered to be responsible for this case.
Follow-Up Studies ; Hand ; Hearing Loss ; Hearing Loss, Sudden* ; Humans ; Vertigo* ; Vestibular Neuronitis* ; Virus Activation

Human bocavirus 1 (HBoV1) non-structural protein NS1 is a multifunctional protein important for virus replication and induction of apoptosis in host cell. To better understand the function of the NS1 protein, it is urgent to address reducing the toxicity of NS1 to host cells. In the present study, we established a stable cell line that regulates expression of NS1 of HBoV1. The recombinant lentivirus plasmid containing a regulatable promoter fused with ns1 gene was constructed and transfected into HEK 293T cells using transfection reagent. The HEK 293T cell lines stably expressing NS1-100 and NS1-70 proteins were established by screening resistant cells with puromycin and inducing NS1 expression with doxycycline. The expression of NS1 protein was determined by fluorescent labeling protein and Western blotting. HBoV1 promoter was transfected into stably expressing NS1 cell line and its trans-transcriptional activity was analyzed. The results showed that NS1 protein was expressed stably in the established cell lines and had a strong activation activity on the HBoV1 promoter driving luciferase gene. Taken together, this study provides a solid basis for further research on the function of NS1 and the pathogenesis of human bocavirus.
Human bocavirus ; Promoter Regions, Genetic ; Transcriptional Activation ; Viral Nonstructural Proteins ; Virus Replication

Objective: To investigate herpesvirus infection in early stage of hematopoietic stem cell transplantation (HSCT) by multiplex polymerase chain reaction (PCR), and to explore the association between multiple herpesviruses infection and clinical characteristics in HSCT patients and its impact on post-transplant complications and prognosis. Methods: A total of 734 peripheral blood samples were collected from 90 patients undergoing HSCT in the Department of Hematology, the First Affiliated Hospital of Soochow University between February 2017 and August 2017. The peripheral blood specimens were obtained before and within 90 days after transplantation at different time points. Lab-Aid824 Nucleic Acid Extraction Mini Reagent was used to extract DNA and multiplex PCR assay was used to simultaneously detect 8 kinds of human herpesviruses from genomic DNA. The incidence of various herpesvirus infections, its correlation with clinical features and effects on post-transplant complications and prognosis were analyzed. Results: The median follow-up time was 192 (range: 35-308) days. Among the 90 patients before transplantation, the incidence of herpes virus infection was 35.6% (32/90), including 12.2% (11/90) with one herpes virus infection and 23.3% (21/90) with multiple viruses infection. The incidence of herpes virus infection after transplantation was 77.8% (70/90), including 20.0% (18/90) with one herpes virus infection and 57.8% (52/90) with multiple herpes virus infection. Among the 52 patients with multiple herpes viruses infection, 30 (57.7%) patients were infected by 2 kinds of viruses, 18 (34.6%) patients by 3 kinds of viruses and 4 (7.7%) patients by 4 kinds of viruses. There was a correlation between HHV-6 and HHV-7 herpesvirus infection (OR=13.880, Q=0.026). EBV infection was related to HHV-7 infection (OR=0.093, Q=0.044). The age of patients was correlated with the incidence of HHV-1 infection before transplantation. There were 24 patients in our study experienced clinical symptoms associated with viral infection. The main manifestations were hemorrhagic cystitis (HC), interstitial pneumonia, enteritis, viral encephalitis and fever of unknown origin. EBV infection was related to HLA incompatibility and the inconsistent of the ABO blood group and grade Ⅱ-Ⅳ aGVHD after transplantation. HLA incompatibility and the unrelated donor and grade Ⅱ-Ⅳ aGVHD were related to multiple viruses infection. Conclusion: Multiple herpesviruses were common in patients undergoing HSCT, which were closely related to HLA mismatch, unrelated donor and grade Ⅱ-Ⅳ aGVHD.
DNA, Viral ; Hematopoietic Stem Cell Transplantation ; Herpesviridae ; Herpesviridae Infections ; Humans ; Multiplex Polymerase Chain Reaction ; Virus Activation

B-Lymphocytes ; immunology ; Hepatitis B ; complications ; Humans ; Liver Transplantation ; adverse effects ; Lymphocyte Activation ; Lymphoproliferative Disorders ; etiology ; Male ; Middle Aged ; Risk Factors ; Virus Activation

No abstract available.
Antiviral Agents/*therapeutic use ; Colitis, Ulcerative/*drug therapy ; *Cytomegalovirus ; Cytomegalovirus Infections/*drug therapy ; Ganciclovir/*therapeutic use ; Humans ; *Virus Activation

No abstract available.
Antiviral Agents/*therapeutic use ; Colitis, Ulcerative/*drug therapy ; *Cytomegalovirus ; Cytomegalovirus Infections/*drug therapy ; Ganciclovir/*therapeutic use ; Humans ; *Virus Activation

Allergens ; immunology ; Animals ; Asthma ; etiology ; Enzyme Activation ; Lung ; pathology ; Matrix Metalloproteinases ; physiology ; Mice ; Respiratory Syncytial Virus Infections ; enzymology ; pathology

Occult HBV infection (OBI) is defined as presence of HBV DNA in the liver tissue in patients with serologically undetectable HBsAg. There are differences in virologic and serological profiles of OBI. Majority of OBI are positive for anti-HBs and/or anti-HBc and minor portion are negative for all HBV markers. However, there are no HBV mutations in the surface and its regulatory regions. HBV infection persists by the presence of covalently closed circular DNA (cccDNA) within the infected hepatocytes, which serves as a reservoir for future infection. OBI increases the risk of HBV transmission through transfusion, hemodialysis, and organ transplantation. Therefore effective measures should be employed to screen OBI. Antiviral therapy is needed in HBsAg-negative transplant patients who are anti-HBc positive to prevent the recurrence of HBV infection. Since HBV replication is strongly suppressed by immune surveillance system in OBI patients, immunosuppression results in massive HBV replication. This leads to acute hepatitis and sometimes mortality when immune surveillance is recovered after stopping immunosuppressive drugs/anticancer chemotherapy. Therefore, narrow surveillance is required to recognize the viral reactivation and start antiviral agents during immunosuppressive therapy/anticancer chemotherapy in patients with OBI.
Blood Transfusion ; DNA, Viral/analysis ; Hepatitis B/*diagnosis/transmission ; Hepatitis B Core Antigens/immunology ; Hepatitis B virus/genetics/*physiology ; Humans ; Liver Transplantation ; Renal Dialysis ; Virus Activation