“…Although Dulbecco et al eliminated several explanations, e.g., dissociation, participation of nonantibody serum components, and hereditary heterogeneity, a positive explanation had yet to be found. Subsequent studies indicated that this phenomenon was characteristic of a wide variety of viruses (Wallis and Melnick, 1967), e.g., picornavirus (Dulbecco et al, 1956;Mandel, 1958;Bradish et al, 1962;Wallis and Melnick, 1965;Ozaki, 1968;Fiala, 1969;Lewenton-Kriss and Mandel, 1972), myxovirus (Lafferty, 1963a,b), paramyxovirus (Granoff, 1965), poxvirus (Lafferty, 1963a,b ;McNeill, 1968;Majer and Link, 1970), togavirus (Dulbecco et al, 1956;Hashi-mot0 and Prince, 1963;Rawls et aE., 1967;Ozaki and Tabeyi, 1967;Westaway, 1968;Hahon, 1970b;Symington et al, 19771, herpesvirus (Yoshino and Taniguchi, 1965b), equine arteritis virus (Hyllseth and Petterson, 19701, reovirus (Huggett et al, 1972), and bacteriophages (Hale et al, 1969;Rappaport, 1970). Kjellh (1962) observed a gradual increase in resistance to neutralization the longer adenovirus reacted with antiserum.…”