3 Experimental Biology and Assay of Retroviruses

Abstract

I. INTRODUCTION
As with other animal viruses, the molecular biology of retroviruses has depended on the use of experimental laboratory procedures for the isolation, propagation, assay, and cloning of biologically active virions. The development of monolayer and suspension cell-culture systems has played a crucial role in experimental biology of retroviruses.

The replication of retroviruses need not kill the host cell. The maturation of viral particles by budding from the plasma membrane does not usually cause cytopathic effects; therefore, an infected cell can become transformed and proliferate while producing virus progeny. However, as Temin (1963) first reported, virus replication is not necessary for cell transformation; neither is cell transformation necessary for virus replication (see Fig. 3.1). These phenomena are discussed in detail in later sections.

Originally, the retroviruses were classified according to the disease that they caused and were named after their discoverers. C-type RNA tumor viruses may be broadly divided into sarcoma and leukemia (leukosis) viruses. The division is not a clear one because some leukemia viruses can also produce a wide spectrum of solid tumors (see Chapter 8). Also, leukemia viruses are commonly present in stocks of sarcoma viruses, and src deletion mutants (transformation-defective [td] viruses) of nondefective avian Rous sarcoma viruses (RSVs) are leukemogenic. Sarcoma viruses transform fibroblasts in culture, and cell transformation is the criterion by which these viruses are usually assayed. Avian leukemia viruses (ALVs) do not usually transform fibroblasts, although they readily infect and replicate in them. Some acute, defective leukemia viruses transform fibroblasts (e.g...