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The development of viral antigen detectable by the fluorescent antibodytechnique and the production of infectious virus were studied iua Vero and E. Derm(NBL-6) cells infected with equine arteritis virus. In both cells the latent period lasted10 to 12 hr, followed by an exponential increase of infectious virus, and the peak Literwas reached 16 to 24 hr after infection. Viral antigen appeared as a small number ofgranules in the perinuclear region of the cytoplasm as early as l0hr after infection ina few cells. Fourteen to 16hr after infection, viral antigen filled the cytoplasm. At 24hr, cell rounding was found in fluoresced cells and some cells became detached from the glasswall. Viral antigen was detected exclusively in the cytoplasm. Although the above find-ings were common in both cells, the intensity of fluorescence was stronger in the E. Derm(NBL-6) cells than in the Vero cells.

Adeno 7 virus replicated well in human diploid (LEP) cells but only to a low degree in green monkey kidney (GMK) cells at 37° C; it did not replicate in either system at 29° C. At 37° C SV40 virus replicated well in GMK cells but only moderately in LEP cells; at 29° C it did not replicate in either system. SV40-adeno 7 hybrid grew in both GMK cells and LEP cells at 37° C. At 29° C this virus replicated in GMK cells but not in LEP cells. While the formation of V-antigen generally corresponded to the infectious virus production in the respective system, considerable differences were encountered in the T-antigens production. Adeno 7 T-antigen was detected earlier and in a higher percentage of GMK cells than in the fully permissive LEP cells and its formation was only slightly influenced by the incubation temperature. SV40 T-antigen was more efficiently formed in GMK cells than in LEP cells. At 29° C SV40 T-antigen was only found in GMK cells and was detected later than at 37° C. The difference in the formation of SV40 T-antigen in GMK cells infected with SV40 and SV40-adeno 7 hybrid virus was further analyzed. The results obtained suggest that an early step of the virus-cell interaction, but neither virus attachment nor penetration, was involved.

Infectious pancreatic necrosis virus was stable for 10 days at 4 C in stream and well water, after which the virus had a half-life of 7.5 days. At 15 C, the virus was stable for 5 days, and then had a half-life between 5 and 6 days. Viral antigen in infected cells developed much more slowly at 4 C than at 20 C. Infected cells released infectious viral particles at temperatures as low as 4 C. Nutrition had a greater effect on the production of infectious virus at 4 C than at 20 C.

Immunity against Marek's disease was conferred by the use of non-infectious materials extracted with non-ionic detergents from cells infected with the attenuated strain of Marek's disease virus (MDV). Antibody-free Rhode Island Red chicks were inoculated at 1 week of age with cell extracts emulsified in Freund's complete adjuvant and were given a second inoculation 1 week later without adjuvant. Protection against natural infection was obtained in groups inoculated with both soluble (not sedimented at 100,000 times g/2h) and insoluble antigens present in Nonidet P40 (NP40) extract, but only with the insoluble fraction of deoxycholate extract. The results suggest that the immunizing antigens can be partially solubilized with 0.5% NP40 and that the growth and spread of MDV are reduced in immunized chickens.

1. 1. Bacteriophage ϕ6 can produce plaques at temperatures up to about 30 °C. Above this temperature (31 or 32 °C), infected cells do not lyse. Temperature shift and pulse experiments ( 25 → 31 ° C , 31 → 25 ° C, and 31 → 25 → 31 ° C ) indicate that this temperature sensitivity for production of infectious virus particles occurs very late in infection and is reversible. 2. 2. The use of spin-labeled hydrocarbons to probe the membranes of host cells and virus indicates the occurrence of a “phase transition” in both cellular and viral mambrances at about 30 °C. 3. 3. The phospholipid composition of infected cultures (at 25 or 31 °C) very late in infection is intermediate between that of uninfected cells and purified virus. 4. 4. These results are discussed in relation to the assembly of ϕ6 membrane components.

Transformation of a clonal line of BHK21 cells by type 12 adenovirus (Ad 12) is described. A transformation rate of approximately 2 × 10−5 per initially infected cell was observed after high multiplicity infection. A study of the fate of the abortively infected cells revealed, however, that only a small fraction survived the infection and initiated growth of a colony. Of these rare surviving colonies, nearly half contained transformed cells. Of three BHK21 sublines tested, one yielded transformed cells only from colonies growing in soft agar suspension, a second yielded transformants only as foci in monolayers, while the third did not yield detectable transformants by either method. The adenovirus-transformed cells were distinguished from the parental BHK21 cells by the following characteristics: The latter property is most likely due to blockage of a step late in the adenovirus replicative cycle, since 88% of the cells, which synthesized Ad2-specific structural antigens did not yield infectious virus. A similar shift from a productive to a largely abortive response to Ad 2 was seen in BHK21 cells simultaneously infected with Ad 12 and Ad2. This finding supports the view that the restriction of Ad2 replication in Ad 12-transformed cells, like the other characteristics mentioned, is associated with continued activity of at least part of the Ad12 genome.

Infectious virus may be isolated from SV40-transformed human cells during the early stages of transformation.1, 2 However, no virus can be detected in the majority of human cell lines after recovery from the crisis period.3 In transformed green monkey kidney (GMK) cells, following abortive infection with SV40, infectious virus cannot be recovered at all.

Homologous autointerference in VSV varies greatly with different host cell cultures. “High-interference” hosts show extensive inhibition of infectious virus replication in the presence of defective interfering particles (DI), while “low interference” hosts do not. The absence of interference in the latter is not due to an inability to produce DI but to a lack of susceptibility to interference by DI. Our working stock of New Jersey VSV exhibits a single size class of DI particles on sucrose gradients. Although the RNA of the standard infectious particle appears to be homogeneous in size, DI RNA is clearly heterogeneous. Single plaque isolates were found to generate several distinct size classes of DI which also contain heterogeneous RNA. The DI produced from a working stock of Indiana VSV on the other hand appear to contain homogeneous size RNA, as other investigators have reported.

Concanavalin A (Con A) has been used to rapidly and selectively agglutinate murine and avian oncornavirions from culture medium or plasma. The agglutinated virus was concentrated rapidly and gently by low-speed centrifugation and solubilization with α-methyl mannoside. Infectious virus was purified 2.3 times with respect to nucleic-acid content, and more than 60% of its infectivity was recovered. Infectious particles of densities 1.18 and 1.16 g/cm 3 were found in mouse cells infected with Friend virus. Con A reacted only with particles of density 1.16 g/cm 3 , indicating heterogeneity with respect to carbohydrate content or structure as well as buoyant density. Electron microscopy of virus agglutinated with Con A showed a zone of Con A-glycoprotein complexes averaging 12-15 nm in thickness.

SummaryA method is described whereby it was possible to rapidly and quantitatively determine the number of competent host cells infected in monolayer culture with myxoviruses. Fowl plague virus and Newcastle disease virus were compared with respect to thier ability to form infectious virus at various multiplicities of infection. It was also shown, that specific antiserum, if present throughout the multiplication period, did not interfere with the final test results.

The infective titer of reovirus could be increased 4–8 times by heating at 50–55° for 5–15 minutes in 2 M MgCl 2 . Virus which could be thermally activated was produced early as well as late in the growth cycle. Only Mg ions have been found to enhance the titer of reovirus at 50°; other divalent cations and NaCl were without effect. While the titer of infectious virus could be increased, the titer of viral hemagglutinin remained the same as that of the unheated samples. Conversely the infectivity of the virus could be reduced and its hemagglutinin destroyed by exposing the virus to subzero temperatures in 2 M MgCl 2 or other divalent salts. Dispersion of the virus particles by heat and aggregation by cold did not play a role in the peculiar responses to temperature changes found for reovirus. The small fraction of the virus population (less than 0.1%) resistant to cold temperatures continued to yield progeny that were almost all cold-susceptible in the presence of MgCl 2 .

Quality measurements (number of virions per plaque forming units) were made on vesicular stomatitis virus indicating a virion: p.f.u. ratio of approximately 1. This highly infectious virus was produced by careful control of the inoculum size to avoid the production of the small inhibitory particles associated with VSV. The effect of virus aggregation on titer was investigated, as well as the effect of the dispersal techniques on viral infectivity. Thermal inactivation studies at various temperatures ranging from −57°C to 56°C showed the virus to be relatively stable when stored as a cell lysate or diluted 1∶:10 in nutrient media.

SummarySuspensions of Polioviruses Types I, II and III in medium 199 derived from infected monkey kidney cell cultures were not completely inactivated following exposure for 1 hour to temperatures of 60° and 65°C. In one instance infectious virus was demonstrated in a suspension of Poliovirus Type II after heating at 75°C for 1 hour. Progeny of virus surviving at this temperature exhibited increased thermoresistance.

Chemically mutagenized populations of vesicular stomatitis virus (VSV) were screened for two general classes of conditional lethal viruses. Host-restricted ( hr ) clones that were unable to elicit productive infections in nonpermissive HeLa or HEp-2 cells were selected from small plaques formed on mixed indicator cultures of chick embryo fibroblasts and HeLa cells. Most of these hr mutants also displayed a temperature-sensitive ( ts ) phenotype in permissive CEF cells. Evidence for the existence of spontaneous VSV hr mutants was obtained. The majority of the ts clones selected in CEF cells by conventional methods lacked the hr marker. Specific hr and ts mutants could be distinguished from wild-type virus on the basis of increased thermolability of their infectivity or diminished in vitro activity of their virion-associated transcriptase. Tests for the ability of these mutants to promote virus-specific RNA synthesis under nonpermissive conditions in cells treated with actinomycin D established the following relationships: (a) both “RNA + ” and “RNA − ” classes of mutants were found when infections were carried out in permissive cells incubated at temperatures restrictive for growth of ts phenotypes; (b) all clones possessing the hr marker failed to induce significant uridine incorporation (“RNA − ”) in nonpermissive HEp-2 cells incubated at high or low temperatures; (c) all mutants scored as “RNA − ” types when infections were carried out in nonpermissive HEp-2 cells at restrictive temperature irregardless of their phenotype for the hr and ts markers.

Studies correlating the production of infectious adenovirus (types 5 and 7) and the progression of the stages of virus-induced cytologic change in HeLa cells are presented. The results reveal a close relationship between the development of the characteristic nuclear changes and adenovirus synthesis. They suggest that cells manifesting the first stages of nuclear change, characterized by the appearance of eosinophilic, Feulgen-negative inclusions, contain little or no mature infectious virus, whereas cells in the later stages, with Feulgen-positive and basophilic inclusions, contain relatively large amounts.

Viruses were isolated from sheep faeces using lamb kidney cultures and examined by negative contrast electron microscopy. Nine agents were morphologically indistinguishable from adenoviruses and their physical and chemical characteristics were also constistent with those of agents of the adenovirus group. Antiserum to 3 of the 9 isolates was prepared and cross neutralisation tests indicated that the 3 were serologically distinct. However 5 of the 6 remaining agents were related to the prototype strains. The sixth strain produced little infectious virus and was not typed.

Cis-dichlorodiammineplatinum (II) partially inhibits the replication of SV 40 virus in green monkey kidney cells. The results of both immunofluorescence and complement-fixation tests indicated that the production of the T antigen of SV 40 was unaltered, but V antigen production was suppressed. The partial block of V antigen synthesis was most marked in the early period after infection, subsequently it was less pronounced. Both infectious virus production and V antigen formation were most markedly inhibited in cells treated with DDP both before and after infection.

An established cell line derived from the ovary of adults of the cotton bollworm, Heliothis zea , supported growth of the Heliothis nucleopolyhedrosis virus (NPV). Typical NPV symptoms were obtained when infected cells were fed to neonatal bollworms; however, the cell line never produced free virions or inclusion bodies containing virions. Infectious virus was passed through the cell line 7 consecutive times, using only infected cells from the previous pass. Infectivity at the 7th serial-pass represented a dilution of >10 −8 of the original inoculum.

SummaryPotassium ion augments the amount of infectious Coxsackie B2 virus produced from MKC and MTC. Production of infectious Coxsackie B2 virus was reduced 500 to 2,000 times in MKC and MTC by depletion of potassium from their medium. Similar results were not obtained with Coxsackie B3 virus. Potassium was not required for virus attachment, but did stimulate glycolysis of tissue culture cells. Potassium could be replaced in a deficient medium after 12 hours of infection and still obtain maximal yields of infectious virus in MTC.

The spread of infectious virus in the tissues of mice after infection with two serologically very similar plaque mutants of Mengo virus has been determined at daily intervals. The distribution of L-Mengo (a large-plaque, virulent mutant) after intraperitoneal and intravenous administration was quite similar, indicating that after intraperitoneal injection this mutant spreads throughout the animal by way of the vascular system. Infectious virus was recovered from all tissues examined except the liver. In contrast, S-Mengo (small-plaque, avirulent) was recovered only from the spleen and lymph nodes after either intravenous or intraperitoneal injection. After intravenous injection, L-Mengo was cleared only very slowly from the bloodstream and at a rate similar to that of two strains of poliovirus. On the other hand, intravenously injected S-Mengo was completely cleared within 30 min. Starting at around 4 h post-inoculation, high titers of interferon were induced in the serum by L-Mengo, reaching a peak by 12 h and remaining elevated for at least another 12 h before declining. Since little or no interferon was found in the serum after intravenous injection of S-Mengo, heat- or ultraviolet-inactivated L-Mengo, or poliovirus types 1 and 3, it was concluded that the presence of circulating, replicating virus was required for induction. The significance of these results is discussed.

The buoyant density of the Bucyrus strain of equine arteritis virus was studied by isodensity centrifugation on three types of gradients. The distribution patterns of infectivity were dependent on the type of gradient used. In sucrose gradients a single peak of infectivity at densities approximating 1.17 g/ml was obtained. From this gradient the total recovery of infectious virus varied between 80 and 90%. In cesium chloride gradients a rather broad band appeared in the form of a “saddled” peak with a range of densities from 1.180 to 1.215 g/ml, the total recovery being 90%. In potassium tartrate (KT) gradients two peaks were formed, one at 1.17 and another at 1.24 g/ml; the total recovery was 50%. Recentrifugation of fractions from KT gradient on sucrose gradients resulted in a changed distribution of infectivity for particles of higher density (1.24 g/ml).

Titers of vaccinia virus consistently increased in cultures of washed phytohemagglutinin-treated, peripheral blood leukocytes of a vaccinated adult. Concomitantly, a gradual rise occurred in the numbers of infected leukocytes, as determined by the infective center assay. Increase in viral titer was accompanied by cell injury, decline in cell numbers, and decreased acid production. Leukocytes not pretreated with phytohemagglutinin appeared to form infective centers after exposure to the vaccinia agent, but they did not replicate infectious virus. For viral replication, the continuous presence of phytohemagglutinin was required.

By heating neutralized mixtures of type 1poliovirus and antibody at 50° in 2 m Cad 2 or MgCl2, the virus could be dissociated from its antibody, and 100 %recovery of infectious virus could

Most influenza viruses are inconsistent and unreliable in their plaque-forming capacities, and this has long been a major handicap in basic research. Only strains of fowl plague virus and the human type A variant (WSN) are consistently good plaque producers and, for this reason, have received an undue amount of attention in influenza virus genetics. In attempts to widen the scope for other strains, the following primary tissues have been investigated, chick embryo fibroblasts (Granoff, 1955; Simpson & Hirst, 1961), calf kidney (Lehmann-Grube, 1963), hamster kidney (Grossberg, 1964), monkey kidney (Choppin, 1962; Vonka, 1965) and chicken kidney (Babiker & Rott, 1968). Although individual workers have reported success with their own particular methods, their techniques have frequently been unreproducible and it has often been necessary to accept low rates of plaquing efficiency and to subject viruses to long processes of tissue adaptation. Continuous cell lines have presented even greater problems since most of them do not yield infectious virus.

Progress in the study of adenoviruses has reached a level that may justify an attempt to define and classify them. For this purpose, the Virus Subcommittee of the International Nomenclature Committee appointed a study group to prepare a statement on adenoviruses in accordance with the system agreed upon during the VIIIth International Congress of Microbiology in August, 1962. This system is based mainly on the chemical and structural characterization of the infectious virus particle or virion. As only a relatively small number of adenovirus types have been adequately investigated in this respect, the inclusion of viruses in the group has been based in the past mainly on the criteria established by Rowe et a1. (1955)) namely ether resistance, behaviour in tissue cultures, production of a group-specific soluble antigen, and lack of pat’hogenicity for laboratory animals. In the present description it is accepted that failure of a given virus to fulfill these crit,eria does not justify its exclusion from the group, provided it can be shown to conform to the basic chemical and structural characterization of adenoviruses. The group is divided, according to natural hosts, into 6 subgroups represented by human, simian, bovine, canine, murine, and avian adenoviruses. This arbitrary classification may require modifications in the future, especially since possibIe antigenic relationships between serotypes belonging to different subgroups are still to be excluded. Further invest,igations of this point is highly desirable. Several of the subgroups of adenoviruses can be further divided into a number of types on the basis of type-specific serological tests. A total of 44 types have been identified so far, and this number is almost certain to increase in the future. A survey of the literature is beyond the scope of the present report, and for this, reference is made to review articles by Enders et ul. (1956)) Hilleman (1957)) Hueb;, ner et al. (1957,1958), Pereira (1959) i Gins: berg (1962)) and Rowe and Hartley (1962).

Spendlove, Rex S. (California State Department of Public Health, Berkeley), Edwin H. Lennette, Charles O. Knight, and Jean N. Chin . Production in FL cells of infectious and potentially infectious reovirus. J. Bacteriol. 92: 1036–1040. 1966.—A comparative study was made of the development in, and release from, FL cells of infectious and potentially infectious (chymotrypsin-activatable) reovirus (Lang strain). The latent period was shorter, the rate of synthesis was more rapid, and the total yield was more than 10-fold greater in potentially infectious virus as compared with infectious virus. Almost all of the potentially infectious virus, but only approximately one-third of the infectious virus, was released from the infected cells.

Hamster embryo fibroblasts were transformed by the SV40-Adeno 7 hybrid virus. The transfomed cells, denoted KE SP2, contained the SV40 tumor (T) antigen demonstrable by both complement-fixation reaction and immunofluorescence tests, but no infectious virus. Attempts to rescue the SV40-derived marker from the transformed cells failed. The KE SP2 cells induced tumors in adult hamsters; sera from these animals contained antibodies reacting with the SV40 T antigen, but not with the SV40 or Adeno 7 viral (V) antigens. Immunofluorescence tests with monkey kidney cells infected with the prototype Adeno 7 (Gomen) virus revealed also the presence of antibodies reactive with the Adeno 7 T antigen. Cells containing the determinant for its synthesis were not lost after one passage in hamster or after a long history of passagesin vitro.

The effect of 5-iodouraoil deoxyriboside on the infective process in rabbit kidney cells infected with pseudorabies virus was investigated. Under the experimental conditions used, viral DNA is formed in which approximately 90% of the thymidine is replaced by 5-iodouracil deoxyriboside. Viral proteins are also synthesized by the virus-infected, drug-treated cells; however, the formation of viral particles does not occur in these cells. The lack of formation of viral particles is not due to a distortion of the DNA molecule (resulting from the presence of the drug) which prevents the enclosure of this DNA into viral coat proteins. This was concluded from the fact that viral DNA containing 5-iodouracil in both strands can be assembled into viral particles, if thymidine is supplied to the infected cells at some time during the infective process. The presence of thymidine during the early stages of infection also increases the yield of infectious virus. Evidence that these infectious viral particles contain 5-iodouracil in their DNA was provided by the fact that they are more sensitive to irradiation with 60 Co than normal, infectious viral particles. It is concluded that viral DNA containing 5-iodouracil causes the synthesis of non-functional proteins involved in virus assembly. This DNA can, however, initiate the infective process and upon replication give rise to normal thymine-containing DNA.

The abortive infection of G1-arrested BHK21 cells with type 12 adenovirus (Ad12) has been shown to induce a 3- to 5-fold increase in the rate of uridine- 3 H incorporation into RNA, with a time course parallel to that of the induction of cellular DNA synthesis. Neither of these responses occurs in the absence of infectious virus. Uridine kinase activity is increased at the same time. Sucrose gradient analysis of the RNA has revealed that 45 S, 32-28 S, 18 S, and 4 S species of cellular RNA are all synthesized at an increased rate. Hybridization studies have demonstrated that Ad12-specific RNA is also synthesized. Its synthesis is first detectable at 10 hr and reaches a maximum at 12–14 hr after infection. It sediments in the 18 S region of the sucrose gradient and is presumably virus messenger.

Growth of a cloned stock of rabbitpox virus in the presence of the mutagens 5-bromodeoxyuridine and 2-aminopurine resulted in a reduced yield of infectious virus. Temperature- and host-dependent mutants could be detected in these yields. Methods were devised for the large-scale isolation of both types of conditional lethal mutants and for enriching the yield of temperature-sensitive mutants by the use of the viral inhibitor isatin β-thiosemicarbazone.

Highly infectious tobacco mosaic virus (TMV) has been reconstituted in vitro with an anomalous noninfectious protein isolated from diseased plants and nucleic acid isolated from tobacco mosaic virus. It appears then that virus biosynthesis occurs in two parts: by the reduplication of virus nucleic acid and the formation of an anomalous protein. In the host, these components are produced separately and simultaneously; then under the proper conditions they polymerize to constitute the characteristic rod-shaped infectious virus particles.

Durand , D. P. (University of Missouri, Columbia). Interference between viable strains of Newcastle disease virus. J. Bacteriol. 82: 979–983. 1961.—Strains of Newcastle disease virus (NDV) which differed in their ability to produce plaques on monolayers of chicken embryo cells were studied during conditions of dual infection. Interference with NDV plaque formation by a nonplaque-forming NDV strain was observed. The primary mechanism involved with this type of interference appears to be due to the viable infectious virus, and is not associated with interferon production or the hemagglutinin of NDV.

SummaryThe CF antigen of ECHO 19 virus can be separated from the hemagglutinin and infectious virus particle. Although the 3 properties, based on sedimentation, indicated a close association, nevertheless, during virus multiplication each emerged at different periods. Infectivity and HA properties were labile to heat and UV irradiation; the CF was stable to both heat and UV. Absorption of infected TC fluid with human “O”erythrocytes removed more than 99% of infectious virus and hemagglutinin. The CF antigen was unaffected by absorption which indicated that the infectivity and HA were more closely combined than the CF. The available data suggested that the CF antigen is an integral part of the virus particle (non-infectious).

The sensitivity of quantal and graded responses to mouse-adapted bluetongue virus for the detection of neutralizing antibody was compared using probit and rankit analysis. The graded response, based on survival times, allowed the demonstration of antibody in highly dilute serum, in which antibody was not detected by the quantal response recording percentage death.Quantal responses to bluetongue virus variants were compared with theoretical dose-response curves constructed according to the Poisson distribution for the random variation of virus particles in inocula. Of these theoretical curves the first term in the Poisson distribution gave the best approximation to the experimental data but the fit to normal distribution curves was better. The quantal responses to bluetongue virus did not appear to reflect the random variation of one-or-more infectious virus particles in inocula.In graded responses to bluetongue virus, a rectilinear relationship was observed between reciprocal harmonic means of survival times and log virus dilutions.

The authors have studied the transmissibility of the virus MHV-3 by the transplacental route from experimentally infected pregnant mice to their fetuses at term, delivered by caesarean section and likewise by the transplacental or vaginal route from the infected mother to mice spontaneously delivered and entrusted to healthy wet-nurses. In both cases, in spite of the severe maternal infection, no virus was detected in the liver of the young. Other experiments have demonstrated the full susceptibility of mice, in the first hours after birth, to the infection experimentally induced by the intraperitoneal incoulation of virus. The obtained results allow the conclusion that infectious virus does not pass to the young by the transplacental or vaginal route.

The multiplication of Newcastle disease virus (NDV) in the allantoic membrane of the chick embryo has been analyzed. About 40 to 80% of the virus inoculated was adsorbed, and of this less than 0.1 to 1% could be demonstrated in the allantoic membrane up to 2 hours after infection. After 2 to 3 hours, virus increased steeply in the allantoic membrane and was rapidly released into the allantoic fluid. Evidence is presented which suggests a continuous virus production for many hours after initial infection. The nonsedimentable, noninfectious hemagglutinin of NDV (S) could be demonstrated early in the infectious cycle but not prior to development of infectious virus. Its presence was confined to the allantoic membrane. Serial passage of undiluted NDV allantoic fluid and inoculation of chick embryos with large amounts of noninfectious NDV (S) did not result in a von Magnus phenomenon. It is suggested that the S hemagglutinin of NDV represents a developmental stage in virus reproduction. A nonsedimentable, noninfectious hemagglutinin has also been demonstrated in the allantoic membranes of chick embryos inoculated with small amounts of PR8 virus. It differs in both biological and physical properties from the noninfectious virus produced by serial passage of undiluted PR8 allantoic fluid and appears to be closely analogous to the NDV S component.