Robert J. Huebner

An avian leucosis group-specific complement fixation reaction. Application for the detection and assay of non-cytopathogenic leucosis viruses

Abstract Sera of hamsters bearing large primary or transplanted subcutaneous fibrosarcomas induced by the Schmidt-Ruppin (S-R) strain of Rous sarcoma virus contain complement-fixing (CF) antibodies reactive not only with the homologous virus, but also with antigens of other avian leucosis viruses. Using this group-specific reaction, a complement fixation test (the COFAL test) was developed for the specific detection and assay of viruses of the avian leucosis group; the test appears to be at least as sensitive and useful as the resistance-inducing factor (RIF) interference procedure. Virus was assayed by inoculating decimal dilutions of virus into chicken embryo fibroblast cultures grown in petri dishes or in roller tubes and testing the inoculated cultures for the development of CF viral antigens. End points for virus assays were obtained in petri dish cultures after one or two cell transfers and also in roller tube cultures without cell transfers. In both systems, virus diluted 10−4 to 10−5 was detected within 10 days of virus inoculation and final titration end points were often reached within 2 weeks. Rous-associated virus (RAV) was readily demonstrated in the Bryan strain but not in the S-R strain of Rous sarcoma virus. The test was effective in demonstrating naturally occurring avian lymphomatosis virus.

Serotype composition of the adenovirus group.

Summary Seven additional adenovirus serotypes of human origin have been established, including a subtype of type 7, designated 7a. Also, 3 additional adenovirus types of simian origin are reported. It is suggested that the adenovirus group be divided into strains of human, chimpanzee, and monkey origin, with separate series of type numbers.

Mouse leukemia virus activation by chemical carcinogens.

The induction of lymphomas in C57BL mice by methylcholanthrene, urethan, or diethylnitrosamine was accompanied by the development of murine leukemia viral antigen in most of the lymphoid tumors. The cell-free transmission of lymphomas induced by methylcholanthrene and the development of antibody to murine leukemia virus prior to the detection of overt lymphoma in these mice suggest that unmasking of a latent leukemia virus is an indigenous actuating cause of the lymphomas.

Outbreak of Febrile Pharyngitis and Conjunctivitis Associated with Type 3 Adenoidal-Pharyngeal-Conjunctival Virus Infection

ON February 11, 1954, a two-year-old girl with acute febrile rhinitis, pharyngitis and conjunctivitis was admitted to the Infectious and Parasitic Disease Service of the Clinical Center at the Nati...

Feline Leukemia and Sarcoma Viruses: Susceptibility of Human Cells to Infection

Human embryonic cells are highly susceptible to infection with feline leukemia and sarcoma viruses. These viruses were propagated in human cultures without antigenic modification or loss of infectivity for cat or human cells. Virus stocks contained at least 106 infectious units of virus per milliliter for human cells. Virus present in 10-6 dilution of virus stock replicated to detectable amounts as early as 7 days after virus infection. The feline sarcoma virus induced morphological transformation of human cells.

Lymphocytic-Choriomeningitis Virus in Hamster Tumor: Spread to Hamsters and Humans

A passage line of a spontaneous hamster fibrosarcoma is contaminated by the virus. of lymphocytic choriomeningitis. Tumors from animals receiving implants when newborn contain high titers of infectious lymphocytic-choriomeningitis virus and complement-fixing antigen, and hamsters receiving implants when weanlings develop high titers of complement-fixing antibody against lymphocytic-choriomeningitis virus. In contrast with the specific reactions of tumorous hamsters to the initiating virus in virus-induced tumors, the development of complement-fixing antibody to lymphocytic-choriomeningitis virus does not depend on the development of tumors. Infant hamsters bearing the tumor have a generalized subclinical infection and seem able to spread virus to other hamsters and to humans.

Demonstration of two immunologically distinct xenotropic type C RNA viruses of mouse cells

Abstract Several independent type C virus isolates were obtained by transplantation of human tumor cell lines into immunosuppressed NIH Swiss mice. Each isolate appeared to be of mouse origin as determined by the antigenicity of its major virion polypeptide, p30. The virus isolates were indistinguishable from each other in serologic and host range properties and also closely resembled BALB:virus-2, one endogenous virus of BALB c mouse cells. However, in immunoassays for a highly type-specific virion polypeptide, designated p12, every isolate was found to differ from BALB: virus-2. These results provide evidence for the existence of immunologically distinct xenotropic viruses of mouse cells.

Differential host range of viruses of feline leukemia-sarcoma complex

Abstract Selected strains of feline leukemia and sarcoma viruses of subgroups A, B, and C show a differential pattern in their ability to cross species barrier and productively infect cells of heterologous host species. A virus of subgroup B showed the widest host range; it caused productive infection of cells of diverse host species including cells from cat, human, monkey, dog, bovine, pig, and hamster species. Two virus strains of subgroup A showed the narrowest host range; of the cells of several mammalian species examined, they only caused productive infection of cat and dog cells. Preliminary studies indicated that certain other strains of subgroup A viruses cause productive infection of whole human embryo cells. One strain of subgroup C virus examined showed a host range that was intermediate between that of A and B subgroup viruses. This strain caused productive infection of cat, dog, and certain human cells. In addition, the subgroup C virus caused productive infection of guinea pig cells found to be resistant to subgroup A as well as subgroup B virus strains examined. Preliminary studies suggested that certain, but not all, virus mixtures of A and B viruses can be purified into B type by passage of virus in heterologous human cells. The factor(s) that may govern the differential susceptibilities of heterologous host cells to the described strains of feline viruses are discussed.

Murine C-type RNA virus from spontaneous neoplasms: in vitro host range and oncogenic potential.

Strain BALB/c mice harbor at least two host range variants of marine leukemia virus. One variant, which is host-cell tropic, is the predominant isolate from neoplastic tissues and produced lymphoreticular neoplasms when injected into BALB/c newborn mice. A second variant, whicht is isolated throughout life, grows poorly in host embryonic cells in culture and was not associated with lymphoreticular neoplasm induction when injected into newborn BALB/c mice.

Serial Propagation of the Guinea Pig Salivary Gland Virus in Tissue Culture

Summary The guinea pig submaxillary gland virus has been successfully propagated in tissue culture, one strain having been carried through 22 serial passages. The tissue culture passage virus produced characteristic intranuclear inclusion bodies in tissue cultures, demonstrated complement fixing and neutralizing antibody responses in guinea pigs infected with animal passage virus, and produced characteristic disease and histopathology in susceptible guinea pigs. Commercial complement consistently contained high titer CF antibody.