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Carcinoma of the true vocal cords is treated in various ways. Hemilaryngectomy is one of these. Unfortunately, this procedure often leaves the patient unable to speak well, and he or she may suffer from aspiration or compromised respiratory function. Five patients with tumor limited to the true vocal cords without cord fixation were treated by hemilaryngectomy with digastric tendon graft insertion in the area of the excised cord. All had reasonable speech facility and no problems with either aspiration of respiratory obstruction postoperatively. Mortality was zero and morbidity was minimal. The technique of digastric tendon graft improves the functional outcome for those patients selected for hemilaryngectomy.

In order to investigate the efficacy of iontophoresis for increasing the penetration of vidarabine monophosphate into the eye, tritium-labeled vidarabine monophosphate was applied to rabbit eyes by topical and iontophoretic application, and the penetration of the compound into the eye, and its subsequent metabolism, were studied. At 20 min after treatment, the ratios of radioactivity for cathodal iontophoresis compared to topical application alone were cornea 8.6, aqueous humor 4.8, and iris 2.4; for 60 min the ratios were cornea 12.2 aqueous humor 17.5 and iris 2.5. In addition, the acid-soluble components were extracted from the cornea and aqueous humor. Vidarabine monophosphate, vidarabine, hypoxanthine arabinoside, adenosine, hypoxanthine, and adenine from the acid-soluble fraction were separated by thin-layer chromatography. The amount of vidarabine monophosphate and vidarabine in the cornea and aqueous humor from the iontophoretically treated group was six to 15 times higher than from the group that received topical application of the drug. It was concluded that cathodal iontophoresis resulted in significantly increased penetration of the antiviral drug vidarabine monophosphate into the anterior chamber of the eye. The effects of iontophoresis of vidarabine monophosphate on corneal epithelium, as observed by scanning electron micrographs, were equal to or less than those seen with the topical application of widely used preservatives in ophthalmic preparations.

Acyclovir and vidarabine exerted a less-than-additive effect on the replication of herpes simplex virus type 1 (HSV-1) in green monkey kidney cells. The synthesis of viral DNA was reduced much more (97%) than that of cellular DNA (45%) by combined acyclovir and vidarabine in cell culture. Furthermore, the combined drugs, given topically or systemically, were more effective than the individual drugs in diminishing the development of clinical signs of HSV-1 infection in hairless mice. However, mortality among animals given topical acyclovir plus vidarabine was not significantly lower than that among animals given topical acyclovir only. Systemic acyclovir (50 mg/kg per day) plus vidarabine (100 mg/kg per day), given for five consecutive days starting 24 hr after viral inoculation, significantly reduced the frequency of development of latent HSV-1 infection in the trigeminal ganglia of mice, whereas systemic acyclovir or vidarabine alone did not.

Vidarabine and L-lysine did not prevent the in vitro reactivation of latent herpes simplex virus or block the further multiplication of reactivated latent virus. Acyclovir and bromovinyldeoxyuridine both blocked the reaction and the multiplication of reactivated latent virus, and transiently suppressed but did not eliminate latent virus from the sensory ganglia.

Systemic treatment of mice with (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) showed a significant therapeutic efficacy against herpes simplex type 1 virus (HSV-1) encephalitis. With treatment initiated 12 h after viral inoculation and continued for 10 consecutive days, BVDU administered intraperitoneally in daily doses of 100-500 mg/kg increased the 21-day survival rates from 30 to 100% and reduced brain virus titers by 3-4 log10 on day 6 post-infection. Furthermore, at doses of 300-500 mg/kg per day BVDU prevented the establishment of latent virus infection in the trigeminal ganglia following intracerebral HSV-1 inoculation.

We studied the effects of herpes simplex virus type 1 (HSV-1) inoculation and topical 7,12-dimethylbenz[a]anthracene (DMBA) application, alone or in combination, on the carcinogenesis and on the amplification and expression of various cellular proto-oncogenes in hamster buccal pouch tissue. Topical DMBA treatment produced tumor formation in pouches, but HSV-1 inoculation, alone caused no neoplastic changes. In pouch tissues receiving both DMBA application and HSV-1 inoculation, the development of initial leukoplakia and tumor has hastened and enhanced in comparison with those receiving DMBA alone. Topical DMBA application to pouch tissue induced an amplification and an increase in the expression of cellular erb-B-1 (c-erb-B-1) proto-oncogene in the epithelial tissue, whereas repeated infection with HSV-1 alone did not. Topical DMBA combined with HSV-1 inoculation, however, resulted in greater amplification and expression of c-erb-B-1 proto-oncogene in the pouch epithelial tissue compared to the DMBA alone. These data indicate that HSV-1 inoculation significantly increases the carcinogenic activity of DMBA, in part, by probably enhancing DMBA-induced amplification and expression of c-erb-B-1 proto-oncogene in hamster buccal pouch tissue.