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

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

We describe a 59-year-old female with severe anticonvulsant hypersensitivity syndrome (AHS) associated with Epstein- Barr virus (EBV) infection. The causative drug was speculated to be carbamazepine. Recurrent EBV infection was demonstrated by the presence of anti-EBV early antigen IgM antibodies and anti-EBV nuclear antigen IgG antibodies. To our knowledge, only one case of drug hypersensitivity syndrome (DHS) associated with EBV has been reported in the English- language literature. Our case is the second report of EBV-associated DHS, which suggests that EBV infection may contribute to the pathogenesis of AHS in a few patients.
Virus Activation/*physiology ; Vacuoles/pathology ; Middle Aged ; Humans ; Herpesvirus 4, Human/drug effects/pathogenicity ; Female ; Erythema/etiology/virology ; Epstein-Barr Virus Infections/*physiopathology ; *Drug Hypersensitivity ; Anticonvulsants/*adverse effects

Antineoplastic Agents ; pharmacology ; Hematopoietic Stem Cell Transplantation ; Hepatitis B ; diagnosis ; prevention & control ; Hepatitis B virus ; drug effects ; physiology ; Humans ; Neoplasms ; therapy ; Virus Activation

To study the expression of herpes simplex virus type 2 latency-associated transcript (LAT) open reading frame 1 (ORF1) and its anti-apoptosis function induced by actinomycin D in Vero cells. The recombinant plasmid pEGFP-ORF1 was constructed and transfected into Vero cells, and the expression of ORF1 was identified by RT-PCR. The changes of Vero cells morphology induced by actinomycin D were observed by fluorescence microscopy, Hochest33258 fluorescence staining. Cells viability was evaluated by MTT assay and cells apoptosis rate was detected by flow cytometry. Double digestion and sequencing confirmed the pEGFP-ORF1 was constructed successfully, RT-PCR showed that the target gene was highly expressed in Vero cells. Hochest33258 staining reaveals that Vero cells transfected with pEGFP-ORF1 and induced apoptosis by actinomycin D had no changes in morphology. MTT assay showed that the viabilities of Vero cells transfected with recombinant plasmid pEGFP-ORF1 and induced apoptosis by actinomycin D has no statistically significant difference compared with the untreated normal control group (P > 0.05), but remarkable higher than Vero cells transfected with empty plasmid pEGFP-C2 and induced apoptosis by actinomycin D, the difference was statistically significant (P < 0.05). Flow cytometry assay shows that the cells apoptosis rate had no significant difference between pEGFP-ORF1 group and the normal group, but the cells apoptosis rate ofpEGFP-ORF1 was lower than the pEGFP-C2 group. HSV-2 LAT ORF1 gene can be expressed in Vero cells and can protect Vero cells from apoptosis induced by actinomycin D.
Animals ; Apoptosis ; physiology ; Cercopithecus aethiops ; Dactinomycin ; Herpes Simplex Virus Protein Vmw65 ; genetics ; Herpesvirus 2, Human ; genetics ; Open Reading Frames ; genetics ; Promoter Regions, Genetic ; Transcription, Genetic ; Vero Cells ; Viral Proteins ; genetics ; Virus Activation ; Virus Latency ; genetics ; physiology

OBJECTIVESTo understand the hepatic pathology, hepatitis B reactivation rates and serological changes in chronic HBV carriers.

METHODSA 5 year dynamic observation and survey of 220 chronic HBV carriers in Wuxi district was taken, analyzing their clinical symptoms, liver histopathology, virology and HBV immunological markers.

RESULTSThirty-five of the 220 (15.9%) patients, showed hepatitis B reactivation. The hepatitis B reactivation rate of patients with obvious hepatic tissue inflammation (> or = G2) was 27.0% (33/122) and the rate of the patients with mild hepatic tissue inflammation (G0-G1) was 2.0% (2/98), showing significant differences (x2=25.41, P less than 0.01). The reactivation rate of patients with high inflammation was clearly higher than those with mild inflammation. Twenty-seven of the 35 hepatitis B reactivation cases were older than 40 years, showing a significant association between the ages of the patients and hepatitis B reactivation rates (x2=6.72, P less than 0.01), moreover there was no relationship between sex and the hepatitis B reactivation rate. There were differences in the inflammation grades and fibrosis stages between HBeAg positive and anti-HBe positive group cases (Kruskal-Wallis Test, x2=8.68, P less than 0.01, x2=6.84, P less than 0.01), showing inflammation grades and fibrosis stages of the anti-HBe positive group were higher than those of the HBeAg positive group. There were no obvious differences about the inflammation grade between age less than 40 years old and > or = 40 years old group cases (x2=0.62, P more than 0.05), but there were significant statistical differences about the fibrosis stage (x2=7.37, P less than 0.01), showing fibrosis stage of more than 40 years old group cases was clearly higher than the less than 40 years old group cases. Fifty-six cases received a liver biopsy for a second time and 23 for a third time. We found those whose hepatic tissues were normal in their first liver biopsies, then their liver histology continued remaining stable for several years while those with abnormal ones hardly or only recovered slightly. The rate of HBsAg turning to negativity per year was 1.55% and for HBeAg was 5.4%.

CONCLUSIONThe hepatic tissue pathology for most chronic HBV carriers (55%) had significant abnormalities (inflammation grade > or = G2), and the rates of hepatitis B reactivation were highly relevant to the liver inflammation grades and the ages of the patients.

Adolescent ; Adult ; Carrier State ; virology ; Child ; Female ; Follow-Up Studies ; Hepatitis B virus ; physiology ; Hepatitis B, Chronic ; pathology ; virology ; Humans ; Inflammation ; Liver ; pathology ; virology ; Male ; Middle Aged ; Virus Activation ; Virus Replication ; Young Adult

BK virus (BKV) is a subtype of papovaviridae. The latent and asymptomatic infection of BKV is common among healthy people. The incidence of BKV re-activation in renal transplant recipients ranges 10%-68%. About 1%-7% of renal transplant recipients will suffer from BKV-associated nephropathy (BKVAN), and half of them will experience graft failure. This paper summarizes the re-activation mechanism of BKV as well as the risk factors, pathology, diagnosis, and treatment of BKVAN.
BK Virus ; physiology ; Humans ; Kidney ; pathology ; virology ; Kidney Transplantation ; Polyomavirus Infections ; diagnosis ; pathology ; therapy ; Postoperative Complications ; diagnosis ; pathology ; therapy ; virology ; Risk Factors ; Tumor Virus Infections ; diagnosis ; pathology ; therapy ; Virus Activation

Measles virus is an enveloped virus with a non-segmented negative-sense RNA genome. Two envelope glycoproteins on the viral surface, namely hemagglutinin (H) and membrane fusion protein (F), are responsible for the virus entry into susceptible host cells. The specific interaction between H and its cellular receptors is a key step in successful virus infection, determining the infectivity and tissue tropism of the measles virus. Thus far, three H receptors have been identified, including the complement regulatory molecule CD46, the signaling lymphocyte activation molecule (SLAM) and the cell adhesion molecule Nectin-4. Here, we reviewed our molecular understanding on the recognition mechanism of these receptors by the viral H protein, aiming to promote future studies on antiviral drug design and measles virus-based oncolytic therapy.
Animals ; Antigens, CD ; metabolism ; Cell Adhesion Molecules ; metabolism ; Hemagglutinins, Viral ; metabolism ; Humans ; Measles virus ; pathogenicity ; physiology ; Membrane Cofactor Protein ; metabolism ; Membrane Fusion ; Membrane Fusion Proteins ; metabolism ; Receptors, Cell Surface ; metabolism ; Receptors, Virus ; metabolism ; Signaling Lymphocytic Activation Molecule Family Member 1