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A case is presented demonstrating the unusual phenomenon of a renal cell carcinoma metastasising to a spinal haemangioblastoma in a patient with von Hippel-Lindau (VHL) disease. Recent advances in the molecular biology of VHL disease relevant to possible mechanisms of tumour-to-tumour metastasis are briefly reviewed.

Argentine hemorrhagic fever is an often fatal human disease caused by Junin virus, an RNA-containing virus and member of the Arenavirus family. This virus was detected in vitro by the polymerase chain reaction (PCR) procedure. A pair of Junin virus-specific PCR DNA oligonucleotide primers and an oligonucleotide probe were designed from a known portion of the viral RNA sequence. RNA was isolated from Junin virus-infected monkey kidney cells and used to produce complementary DNA (cDNA) by reverse transcription. A DNA segment, 151 +/- 24 bp long, was amplified from this cDNA and characterized by agarose gel electrophoresis and Southern blot hybridization with the Junin virus-specific DNA probe. Sensitivity experiments showed that Junin virus could be detected with nanogram quantities of RNA isolated from virus-infected cells. The rapid and sensitive assay described here may contribute towards the development of a procedure for the early diagnosis of Argentine hemorrhagic fever.

The authors determined virus leakage from condoms made from processed sheep caecum using two viral probes simultaneously. They poured a mixture of two viruses, the bacteriophage, phi X174 (4 X 10(7) pfu/ml), and the human pathogen, herpes simplex virus (about 1 X 10(6) pfu/ml), in a buffered solution into condoms, which were suspended into beakers also containing buffered solution. The authors then assayed aliquots from the beakers to measure the extent of virus leakage from the condoms. With one brand of condom, 10 out of 24 samples leaked small amounts of phi X174; with the other brand of condom, 13 out of 24 samples gave similar leakage. The extent of leakage varied over two orders of magnitude from condom to condom within each brand. Of the 23 condoms that leaked the smaller virus, phi X174 (27 nm in diameter), only two also leaked the larger herpesvirus (120-150 nm in diameter). These data demonstrate that (1) large and small viruses can leak from natural membrane condoms; (2) there is considerable variation from condom to condom in allowing leakage of the viruses; and (3) leakage of a small virus does not necessarily indicate that a larger virus will leak from that particular condom. The authors explain some inconsistencies in the published literature.

The capacity of human fibroblasts to support plaque formation by Herpes simplex virus following treatment of the cells with gilvocarcin V, a polyaromatic C-glycoside, plus near ultraviolet radiation (UVA, 320-400 nm) was examined. Gilvocarcin V, plus UVA radiation, effectively inhibited host cell capacity at concentrations five orders of magnitude lower than that of 8-methyoxypsoralen required for capacity inhibition at similar levels of UVA radiation. This result extends the observation of unusual biological potency of UVA-activated gilvocarcins from bacterial cells to human cells.

This article reports three cases of visual failure of presumably ischemic etiology, after aneurysm surgery; the first case occurring 7 months after clipping and gauze wrapping of a 4-mm anterior communicating artery aneurysm; the second case occurring 8 months after gauze wrapping of a partially intracavernous 10-mm internal carotid artery aneurysm which projected into the right optic foramen; and the third case occurring 11 months after ligation, clipping, and gauze wrapping of an 8-mm internal carotid-posterior communicating artery aneurysm.

The existence of untargeted viral mutagenesis in X-irradiated cells was investigated in a mammalian virus/cell system, where a low level of such viral mutagenesis can be demonstrated in UV-irradiated cells. In the positive control experiment UV-elicited mutagenesis was shown with cell exposures of 5, 10 and 15 J/m2 and a delay of 24 h between cell irradiation and infection with unirradiated herpes simplex virus. Although X-ray doses of 1, 3 and 10 Gy elicit enhanced reactivation of UV-irradiated virus, no untargeted mutagenesis for any X-ray dose at post-irradiation infection times of 0, 24 or 72 h was observed in this study. Thus untargeted mutagenesis of herpes simplex virus was not demonstrated in X-irradiated monkey cells, under conditions where X-ray-enhanced reactivation occurs and where untargeted mutagenesis in UV-irradiated cells occurs.

Dyes which photosensitize membranes may be clinically useful for photodynamic treatment (PDT) of Herpes simplex virus (HSV) infections. It is important to determine whether the enveloped HSV can be inactivated via membrane damage without affecting the genetic material. Selection of appropriate PDT conditions, including the choice of dye, could minimize viral mutagenesis. We determined the mutagenesis caused by PDT employing three membrane-photosensitizing dyes of potential use in cancer photochemotherapy (Photofrin II, polyhematoporphyrin esters, zinc phthalocyanine tetrasulfonates) and a DNA-photosensitizing dye (proflavine sulfate). The effects were compared to those caused by exposure of HSV to ultraviolet radiation (UV). The procedure consisted of incubating HSV with microgram/ml (microM) concentrations of the dye, irradiating the samples with broad spectrum visible/near-UV radiation (Daylight fluorescent lamps) and assaying the survival of the treated HSV. Zinc phthalocyanine was the most potent dye per absorbed photon for inactivating HSV. In parallel with determination of survival, progeny of the surviving virus were grown for determination of mutagenesis. The progeny virus was harvested and subsequently assayed in the presence and absence of 40 micrograms/ml iododeoxycytidine (ICrd) to determine the frequency of mutation to ICrd resistance. Mutation frequencies were determined for progeny from the 1-4% survival level. For PDT with each membrane-photosensitizing dye, only zinc phthalocyanine increased the mutation frequency over the untreated control. This increase was less than 2-fold. Proflavine increased the mutation frequency 2-3 fold over the untreated control. Ultraviolet produced a 15-20 fold increase over the untreated control.(ABSTRACT TRUNCATED AT 250 WORDS)

This case of metastatic gestational choriocarcinoma presented as intracerebral hemorrhage from an atypical distal middle cerebral artery aneurysm. Operative evacuation of the intracerebral hematoma was undertaken and histopathological examination revealed choriocarcinoma invading the vessel wall. Neoplastic cerebral aneurysms are unusual, being reported in metastatic choriocarcinoma, cardiac myxoma, bronchogenic carcinoma, and undifferentiated carcinoma. Metastatic choriocarcinoma should be considered in the differential diagnosis of intracerebral hemorrhage in women of child-bearing age. Recent advances in treatment have resulted in a 75% cure rate for metastatic choriocarcinoma.

Enhanced reactivation of Ultraviolet-irradiated virus has been reported to occur in heat-shocked host cells. Since enhanced virus reactivation is often accompanied by untargeted mutagenesis, we investigated whether such mutagenesis would occur for herpes simplex virus (HSV) in CV-1 monkey kidney cells subjected to heat shock. In addition to expressing enhanced reactivation, the treated cells were transiently more susceptible to infection by unirradiated HSV. No mutagenesis of unirradiated HSV was found whether infection occurred at the time of increased susceptibility to infection or during expression of enhanced viral reactivation.

Malmgren, Richard A. (National Cancer Institute; Bethesda, Md.), Alan S. Rabson, Paula G. Carney, and Frances J. Paul. Immunofluorescence of green monkey kidney cells infected with adenovirus 12 and with adenovirus 12 plus simian virus 40. J. Bacteriol. 91:262-265. 1966.-Immunofluorescence studies of the viral antigens and tumor (T) antigens of adenovirus 12 and simian virus 40 (SV40) in green monkey kidney (GMK) cells infected with adenovirus 12 alone or in combination with the SV40 virus showed that the adenovirus 12 viral antigen was produced in detectable amounts only in the cells infected with both viruses. The adenovirus 12 T antigen, on the other hand, was formed in the GMK cells infected with the adenovirus 12 only. This antigen was formed as early as 18 hr after viral infection, and persisted for at least 48 hr after virus infection. There was a correlation between the appearance of the immunofluorescent T antigen in the nucleus and the electron microscope appearance of "nuclear stippling," which developed in the nuclei of GMK cells after infection with adenovirus 12 only, as well as after infection with both viruses.