acyclovir and Carcinoma--Squamous-Cell

Herpes viruses are characterized by their ability to establish and maintain latent infections that can be reactivated. Several stimuli can trigger the reactivation of herpes viruses, which are perhaps best recognized in the recurrent blisters and ulcers associated with herpes simplex virus. We present two clinical cases of reactivation of herpes simplex virus during radiation therapy for management of cancers of the head and neck. Although the role of ionizing radiation in the reactivation of herpes simplex virus has not been established, we review the viral and host events associated with the establishment of orofacial herpes simplex virus infection, latency, and reactivation of the virus. We discuss current models of viral reactivation and suggest directions for further clinical research into the reactivation of orolabial herpes simplex virus during radiotherapy.

Topics: Acyclovir; Adult; Antiviral Agents; Carcinoma, Squamous Cell; Cerebellar Neoplasms; Head and Neck Neoplasms; Humans; Immunocompromised Host; Lymphoma, AIDS-Related; Lymphoma, B-Cell; Lymphoma, Large-Cell, Immunoblastic; Male; Middle Aged; Nasopharyngeal Neoplasms; Radiotherapy; Recurrence; Simplexvirus; Stomatitis, Herpetic; Virus Activation; Virus Latency

Pseudoepitheliomatous hyperplasia (PEH) clinically and histologically mimics squamous cell carcinoma (SCC), specifically in patients with HIV and AIDS.. A 51-year-old G3P2 with AIDS and history of vulvar cancer presented with large bilateral exophytic lesions on the vulva, grossly appearing neoplastic. Initial biopsies of the lesions were interpreted as vulvar SCC. After resolution with empiric treatment with acyclovir for possible herpes simplex virus type 2 outbreak, additional slides were reviewed, and cells with viral inclusions were identified, making the final diagnosis PEH in association with herpes simplex virus type 2 infection.. Although PEH is infrequently encountered, PEH should be considered in the differential diagnosis of vulvar lesions. A multidisciplinary approach including the gynecologist, pathologist, and infectious disease specialists can optimize patient outcome.

Topics: Acquired Immunodeficiency Syndrome; Acyclovir; Carcinoma, Squamous Cell; Diagnosis, Differential; Female; Herpes Genitalis; Herpesvirus 2, Human; Humans; Hyperplasia; Middle Aged; Treatment Outcome; Vulvar Neoplasms

The ability to achieve tumor selective expression of therapeutic genes is an area that needs improvement for cancer gene therapy to be successful. One approach to address this is through the use of promoters that can be controlled by external means, such as hyperthermia. In this regard, we constructed a replication-deficient adenovirus that consists of a mutated herpes simplex virus 1 thymidine kinase (mTK) fused to enhanced green fluorescent protein (EGFP) under the control of the full-length human heat shock (HS) 70b promoter. The virus (AdHSmTK-EGFP) was evaluated both in vitro and in vivo in oral squamous cell carcinoma SCC-9 cells for expression of both mTK and EGFP. The in vitro expression of mTK-EGFP was validated using both (3)H-penciclovir and fluorescence-activated cell sorting assays. These studies show that specific expression could be achieved by heating the cells at 41 degrees C for 1 h, whereas little expression was observed using high doses of virus without hyperthermia. The vector was also evaluated in vivo by direct intratumoral injection into mice bearing SCC-9 xenografts. These studies demonstrated tumor expression of mTK-EGFP after ultrasound heating of the tumors by radioactive biodistribution assays, histology and microPET imaging. These in vivo results, which demonstrate HS-inducible transgene expression using PET imaging, provide a means for noninvasive monitoring of heat-induced gene therapy in local tumors, such as oral squamous cell carcinomas.

Topics: Acyclovir; Adenoviridae; Animals; Antiviral Agents; Carcinoma, Squamous Cell; Cell Line, Tumor; Flow Cytometry; Gene Expression Regulation; Genes, Transgenic, Suicide; Genetic Vectors; Guanine; Head and Neck Neoplasms; Heat-Shock Proteins; Hot Temperature; Humans; Liver; Mice; Mice, SCID; Positron-Emission Tomography; Transplantation, Heterologous

Topics: Acyclovir; Aged; Antiviral Agents; Carcinoma, Squamous Cell; Diagnosis, Differential; Female; Herpes Labialis; Humans; Lip Neoplasms

NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma hybrid cell line (NPC-KT), showed cytopathic changes characteristic of herpesvirus replication, including formation of multinucleated giant cells and inclusion bodies, when Epstein-Barr virus replicative cycle was induced by 5-iodo-2'-deoxyuridine. Acyclovir (an inhibitor of herpesvirus DNA polymerase), Epstein-Barr virus-immune human serum, or 2-deoxyglucose (an inhibitor of the glycosylation) interfered with syncytium formation, indicating that a virus-specified glycoprotein belonging to the late group is responsible for cell fusion induced by Epstein-Barr virus replication in cl.S61 cells.

Topics: Acyclovir; Antigens, Viral; Carcinoma, Squamous Cell; Cell Fusion; Cytopathogenic Effect, Viral; Deoxyglucose; DNA, Viral; Electrophoresis, Polyacrylamide Gel; Herpesvirus 4, Human; Humans; Hybrid Cells; Idoxuridine; Nasopharyngeal Neoplasms; Nucleic Acid Hybridization; Restriction Mapping; Tumor Cells, Cultured; Virus Replication