The Behavior of Different Strains of Poliomyelitis Virus in the Complement Fixation Reaction
Authors: Schmidt Nathalie J. , Lennette Edwin H. , Doleman Jessie H. , Hagens Shirley J. , Dennis Juanita 
Published: January 2023

Discussion and Summary
Although the patients whose sera were examined in this study were from Alameda County, California, they represented 3 different disease years, namely, 1952, 1953 and 1954. The complement-fixing and neutralizing reactivities of the Type 1 virus strains isolated from these patients were compared with the reactivities of the Mahoney strain of Type 1 poliomyelitis virus, a strain isolated more than 10 years earlier in Cleveland, Ohio. The 2 strains of Type 2 virus which were compared for complement-fixing reactivity were isolated in 1953 from a poliomyelitic patient in Alameda County, California, and in 1954 from a case of poliomyelitis in Bernalillo County, New Mexico. The Type 3 viruses were all isolated from patients in Alameda County, but each of the 3 disease years mentioned above was represented.
Much more striking than any acceptable evidence of strain differences uncovered by this study was a similarity of the patients' complement-fixing antibody titers against antigens derived from the standard laboratory strains (Type 1, Mahoney, Type 2, Statler and Type 3, McMullen) and antigens derived from the patient's own infecting virus strain. Thus, of the 217 serum specimens that were tested, in no instance did tests with the patient's own virus as antigen give more than a 4-fold (2 tube) higher complement-fixing antibody titer than did tests with the standard laboratory antigen and a difference of this magnitude was encountered with only 7 or 3.2% of all the specimens tested. It is of interest that although the differences in complement-fixing antibody titer of the sera as measured by antigens derived from the standard laboratory strains and from the patient's infecting strains were slight, in every instance but one in which a difference occurred, the highest titers were obtained against the patient's own virus strain.
Only 3 patients with a Type 1 virus infection and 1 patient with a Type 3 virus infection showed markedly better titers of complement-fixing antibody against their own infecting virus than against the standard laboratory strains. In the case of patient Dennison, the lack of a 4-fold or greater rise in complement-fixing antibody titer in tests with the Mahoney strain antigen would have precluded a serologic diagnosis using this strain, but a 4-fold rise in titer was demonstrable at 21 days postonset when a Dennison strain antigen was used. In the case of patients Hacker, Kaunert and Lower, a serologic diagnosis of poliomyelitis would have been missed with the use of laboratory strain antigens unless very late serum specimens (8 weeks, 12 weeks and 8 weeks, respectively) were tested; this is in contrast to the diagnostically significant rises in antibody titer which were encountered somewhat earlier when antigens prepared from the patient's infecting strain were used, a rise in titer being demonstrable at 21 days for Hacker, at 8 weeks for Kaunert and at 21 days for Lower. In contrast to these 4 patients who had shown no diagnostic rise, or a late rise, in complement-fixing antibody titer in tests against the standard laboratory strain antigens was patient R. Westerfield, who showed no 4-fold rise in complement-fixing antibody titer against either the Mahoney strain or against his own infecting strain; the highest complement-fixing antibody titers attained by this patient were 1:4 as measured by either antigen. The 2 patients who had relatively high stationary complement-fixing antibody titer against the Mahoney strain antigen also showed high stationary titers against their own infecting viruses. Thus, while in 4 patients the diagnosis of poliomyelitis by the complement fixation test was improved or made possible by the use of antigens prepared from the patient's infecting virus, in 3 others laboratory diagnosis was not sharpened by utilizing the patient's infecting virus strain as a complement-fixing antigen.
The studies reported here failed to reveal the existence of any very remarkable differences in complement-fixing capacity between antigens derived from standard laboratory passage strains and those derived from the patient's own infecting virus strain. This suggests that the antigenic make-up of the complement-fixing moiety, at least, is sufficiently similar amongst strains within any immunologic type as to permit use of any suitable strain as an antigen. Additional studies on these aspects, however, are desirable as are inquiries into the possibility that certain strains may be more sensitive or more highly type-specific than others, or give rise to more potent antigens.