Releases of petroleum products from leaking residential storage tanks are a growing problem in the stale of New Jersey. Approximately two releases per day have been reported to the New Jersey Department of Environmental Protection. Product releases may cause aquifers to become contaminated, may affect surface water, or cause vapor problems inside households. As of 1992, there arc no federal or state regulations pertaining to the maintenance and monitoring of residential petroleum storage tanks. Regulations are essential for protecting drinking water supplies. The regulations must address installation procedures, lank materials, monitoring, and tank location.

A 41K early nuclear antigen (p41), expressed in human herpesvirus type 6 (HHV-6)-infected T cells, was cloned by screening a cDNA expression library with the anti-p41 monoclonal antibody (MAb) C5. When expressed in mammalian cells, the cloned p41 protein comigrated with the authentic p41 protein from HHV-6-infected cells and localized to the nucleus. HHV-6 p41 shares 44% sequence identity with the human cytomegalovirus (HCMV) DNA-binding protein, ICP36 (UL44 gene product); p41 binds to ssDNA with the same apparent affinity as ICP36. Since ICP36 has recently been shown to be an HCMV DNA polymerase-associated stimulatory factor, a similar function is suggested for p41.

Human B‐lymphocyte‐derived lines were forced to enter the EBV‐cycle by superinfection with the P3HR‐l substrain of EBV or sodium butyrate treatment. The induced cells were used as targets for natural killing (NK) and EBV‐specific, antibody‐dependent cellular cytotoxicity (ADCC). Two Burkitt lymphoma lines, Raji and Daudi, and one normal adult derived lymphoblastoid cell line, NAD‐7, were comparable in their ADCC‐sensitivity after induction, but only the Burkitt lymphoma‐derived lines showed a major increase in NK‐sensitivity. The superinfection‐induced membrane change, responsible for both NK and ADCC sensitivity, is an early function of the viral cycle, correlated with the appearance of early antigens (EA). Indirect evidence indicates that the NK and ADCC target sites are different but this problem requires further investigation. Sodium butyrate induced an increased NK sensitivity and EBV‐related ADCC sensitivity in the Burkitt lymphoma‐derived P3HR‐l line. Lymphocyte effectors from different donors showed great differences in their NK and ADCC activity. Optimal ADCC could be demonstrated with effectors that were intermediate in their NK‐activity.

We inoculated common marmosets (Callithrix Jacchus) with Herpesvirus ateles (HVA), Herpesvirus saimiri (HVS), and Epstein-Barr virus (EBV). HVA-induced tumors contained several cell types, including giant cells reminiscent of the Sternberg-Reed cells observed in human Hodgkin's disease. HVS and EBV did not induce tumors, although HVS was present in lymphocytes and elicited a strong antibody response. EBV elicited only a variable antibody response. We feel that more common marmosets should be used to determine if the pathologic and immunologic lesions caused by HVA would be a suitable animal model for Hodgkin's disease and/or other malignant lymphomas of man. Inconsistency in the induction of tumors by EBV and HVS in common marmosets suggets that this species may be a different type of model for human cancer research than the cottontop marmoset, which is the most susceptible animal host for EBV and HVS oncogenesis.

Ninety‐five sera from Chinese NPC patients in different stages of the disease, 38 sera from Chinese patients with other cancers, and 50 normal Chinese sera, were titrated for EBNA, VCA, EA and complement‐fixing (CF/S) EBV‐specific antibodies. The geometric mean (GMT) EBNA antibody titre of patients with NPC at stage I was found to be four times higher than that of normal individuals and increased in parallel with clinical deterioration. Antibody titres against EBNA did not correlate with either VCA or EA antibodies but, in general, correlated with CF/S antibodies. EA antibodies correlated relatively well with VCA antibodies and discriminated better than EBNA titre between NPC at stage I and controls.

The indirect immunofluorescent test was used to detect antibodies to herpesviruses types 1 and 2, cytomegalovirus and EBV in sera from patients with cervical carcinoma, condyloma acuminatum and controls from Cali, Colombia, and a control group from the USA. No significant differences were found in the prevalence of antibodies to viral capsid antigens of HSV-1 and CMV among the groups studied. However, titres for HSV-2 were higher in the three groups from Cali (cervical carcinoma, condyloma and controls) than in the control groups from USA. High EBV antibody titres (VCA and early antigens) were found in the three groups from Cali. Antibodies to early antigens of CMV were detected in a sub-sample of the subjects and with higher frequency in patients with cervical cancer. The significance of these findings is discussed.

Oncogenic herpesviruses, like many other viruses, can be concentrated effectively from large volumes of culture fluids by precipitation with methanol with good recovery of infectivity.

Lymphoblastoid cells were cultured from twoHerpesvirus saimiri (HVS) inoculated white-lipped marmosets and from one HVS-inoculated owl monkey. Cells from all three animals grew clumped in suspension. The cells from both species were diploid in chromo-some number and showed no unusual chromosomal abnormalities. The marmoset cell line examined was chimaeric. The marmoset cells lacked HSV-associated antigens as determined by immunofluorescence, and no evidence for the presence of virus was found by either infectivity assays or electron microscopy. Cocultivation of these cells with Vero cells resulted in cytopathology and the recovery of complete, infectious virus. The owl monkey lymphoid cells were positive to a small degree for both viral antigens and infectivity. The cells were resistant to rechallenge with HVS. Cocultivation of these cells with Vero cells led to the development of cytopathology and an increased yield of virus.

Vero cells were infected with Herpesvirus saimiri. Early (EA) and late (LA) viral antigens were distinguished by inhibiting viral DNA synthesis with cytosine arabinoside (Ara C), or allowing it to proceed uninhibited until CPE was visible. The difference in the antigenic specificity of EA and LA was confirmed by direct fluorescence tests, in combination with blocking experiments. Sera that were anti‐EA positive according to the indirect test were capable of blocking the EA staining reaction with direct EA+‐ conjugates, whereas anti‐LA+EA— sera were unable to do so. Healthy adult squirrel monkeys had antibodies to late antigens (LA) but not to early antigens (EA), as judged by immunofluorescence tests. Isolation‐reared, antibody‐free squirrel monkeys responded with anti‐EA and anti‐LA antibodies after HVS inoculation. Uninoculated, cage‐mate squirrel monkeys became infected by horizontal transmission and responded with LA and EA antibodies approximately 2 months after being housed together with the infected animals. Simultaneously isolated controls remained antibody‐free. HVS‐inoculated, tumor‐bearing marmoset and owl monkeys developed antibodies to both LA and EA in the majority of the cases studied, although in some owl monkeys there was only LA and no EA antibody development. Two different patterns of EA staining could be distinguished, trabecular and punctate. There was a conspicuous difference between the species with regard to the timing of antibody development. Squirrel monkeys, the natural host species of the virus, but resistant to its oncogenic action, responded with antibody development within 14–17 days after inoculation. Marmoset and owl monkeys did not respond until 28–80 days. Conceivably, the natural host species has been selected for a high degree of genetic responsiveness against virus‐determined antigens. This may be partly or entirely responsible for its resistance to the oncogenic effect of this virus.

THE inoculation of Herpesvirus saimiri (HVS) heated to 56° C for 30 min into several marmosets (Sanguinus sp.) and an owl monkey (Aotus trivirgatus) has previously been described. No illness was reported following the inoculation1. In our laboratories, two owl monkeys were inoculated with heated HVS shown to be non-cytopathogenic in owl monkey kidney (OMK) and Vero cells. Both monkeys developed malignant lymphoma with lymphogenous leukaemia in a manner identical to animals inoculated with untreated HVS2.

Coronavirus disease (COVID-19) has expanded around the world, resulting in a pandemic with high morbidity and mortality. To date, no specific treatment or vaccine is available to treat or prevent this sudden and potentially deadly disease. Economic restructuring brings opportunities and challenges to integrative medicine treatment. In such complex situations, integrative medicine treatments are to be provided cautiously, and the shift from in-person visits to remote medical services might play an important role in how such services are delivered.

Summary Herpesvirus saimiri (HVS)-induced intracellular and cell membrane antigens were demonstrated in infected owl monkey cells by indirect immunofluorescence methods. Sera from HVS-infected owl monkeys were the source of antibody. The fluorescent reagent was a fluorescein isothiocyanate (FITC)-conjugated caprine antihuman γ-globulin. The effectiveness of the procedure was evaluated on owl-monkey lymphoid cells infected with HVS. Intracellular antigens were detected in infected cells after in vitro cultivation but not in uninfected cells or fresh biopsy material from HVS-infected monkeys. These antigens were demonstrated with post-HVS infection sera from 6 owl monkeys but not with sera taken before or within 5 days after HVS infection. HVS-associated membrane antigens were shown in cells productively infected with the virus. The appearance of these antigens coincided with cytopathogenic changes associated with the viral infection. This was particularly evident in an infected owl-monkey kidney culture where only the rounded cells, not the adherent monolayer, contained both intracellular and membrane antigens. Similar observations were obtained when vero cells, cocultivated with a non-virus-producing marmoset lymphoid cell line, showed cytopathology characteristic of HVS infection. These results demonstrate that membrane antigens are expressed in cells infected with HVS and suggest that their synthesis is a late event in the replicative cycle of this virus.

The WF‐l rat cell line was investigated for the presence of virus‐associated cell membrane antigens similar to those found in the membranes of cells infected with murine leukemia viruses. These cells transform spontaneously in tissue culture from embryos derived from the Wistar‐Furth ( W/Fu) strain of rats and produce large amounts of rat C‐type virus particles. When sera from W/Fu rats bearing WF‐l tumors were tested for antibodies directed against the WF‐l cells by indirect membrane fluorescence, it was found that 20–35% of the cells reacted strongly. The sera did not react with normal W/Fu embryonic fibroblasts nor did absorption of a pooled positive serum with these cells remove antibodies reactive with the WF‐l cell line. Interestingly, however, these sera also reacted with two other virus‐positive cell lines (R‐35 and RMTL‐8) derived from mammary tumors originating in Sprague‐Dawley rats but not with virus‐negative cell lines. Absorption experiments verified that the R‐35 and RMTL‐8 cells contained cross‐reacting antigens with the WF‐l cells. These results suggested that (a) virus‐associated antigens were expressed in the membranes of cells infected with rat C‐type particles and (b) C‐type virus particles found in cell lines originating from different Sprague‐Dawley rats as well as from the Wistar‐Furth strain were antigenically closely related if not identical.

If a substantial reduction in coronary mortality is to be achieved, vulnerable persons will have to be detected and placed under continued surveillance and prophylactic management. The background of the potential coronary candidate has been delineated and a profile capable of estimating risk over a wide range devised. One of the most potent contributors to this profile is the serum lipid value. Although any lipid or lipoprotein can be used, none is more convenient than or superior to a simple total cholesterol determination. For determining the nature of the lipid disorder and choosing the most appropriate therapy, a lipid profile is most useful.