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PubMed1988

Antigenic variation of wild and vaccine rabies strains of Egypt.

Nineteen street rabies virus strains, isolated in Egypt from humans (two), dogs (nine), cats (two), farm animals (two), gerbils (three), and a jackal were antigenically analyzed. The Pasteur strain used for the preparation of human rabies vaccine, the Flury high and low egg passage stains (HEP, LEP) used for animal vaccines, and the challenge virus standard (CVS) strain were also assayed. All were examined by the indirect fluorescent antibody test, using a panel of 20 monoclonal antibodies against the nucleocapsid of rabies and rabies-related viruses. The rabies isolates demonstrated patterns of reactivity with the antinucleocapsid panel different from those of the Pasteur, HEP, and CVS strains. Representative human, dog, and rodent isolates were analyzed by neutralization tests in mice, with a second panel of 19 monoclonal antibodies against rabies and Mokola envelope glycoproteins. With this panel, the isolates demonstrated patterns of reactivity different from the vaccine strains. These data indicate antigenic variation between wild virus and vaccine strains.

Animals↗
PubMed1991

Antigenic variation in Giardia lamblia: infection of congenitally athymic nude and scid mice.

Athymic nude mice of the outbred Zur:ICR-nu and inbred BALB/c strain and scid mice were infected with a cloned human isolate of Giardia lamblia (GS/M-83-H7). Changes in the expression of the major surface epitope of the intestinal trophozoites (characterized by the binding capacity of monoclonal antibody MoAbG10/4) as well as cellular and humoral immune parameters of the hosts were followed during the course of infection. Self-cure was observed in heterozygous (nu/+) BALB/c mice by day 22 post-infection (p.i.) and in heterozygous (nu/+) Zur:ICR-nu strain by day 65 p.i. Homozygous (nu/nu) mice of both strains remained chronically infected until end of the experiments (day 45 p.i. for BALB/c mice and day 122 p.i. for Zur:ICR-nu mice, respectively). Only heterozygous (nu/+) mice were able to mount a gut-associated (Peyer's patch) lymphoproliferative response to G. lamblia antigen. Therefore, T-cell dependent mechanisms were necessary for a self-cure. Antigenic variation occurred in all nu/+ and nu/nu animals of both strains. Trophozoites expressing the major surface epitope (assessed by direct immunofluorescence with FITC-labelled MoAb G10/4) decreased to zero by day 22 p.i. In contrast, the proportion of trophozoites expressing the major surface epitope in infected scid mice remained at the initial level (greater than 99%) until termination of the experiment (day 25 p.i.); therefore, antigenic variation did not occur. All nu/nu and nu/+ mice but not scid mice demonstrated a humoral immune response to G. lamblia antigen. These experiments suggest functional B-cell dependent mechanisms are most likely responsible for the surface antigen switch. Transfer of infection occurred naturally from experimentally infected scid-mice to their mother, proving the initial antigenic surface variant remains unchanged after encystment and subsequent excystment followed by infection in a new host.

Animals↗
PubMed1998

A similar pattern of interaction for different antibodies with a major antigenic site of foot-and-mouth disease virus: implications for intratypic antigenic variation.

The three-dimensional structures of the Fab fragment of a neutralizing antibody raised against a foot-and-mouth disease virus (FMDV) of serotype C1, alone and complexed to an antigenic peptide representing the major antigenic site A (G-H loop of VP1), have been determined. As previously seen in a complex of the same antigen with another antibody which recognizes a different epitope within antigenic site A, the receptor recognition motif Arg-Gly-Asp and some residues from an adjacent helix participate directly in the interaction with the complementarity-determining regions of the antibody. Remarkably, the structures of the two antibodies become more similar upon binding the peptide, and both undergo considerable induced fit to accommodate the peptide with a similar array of interactions. Furthermore, the pattern of reactivities of five additional antibodies with versions of the antigenic peptide bearing amino acid replacements suggests a similar pattern of interaction of antibodies raised against widely different antigens of serotype C. The results reinforce the occurrence of a defined antigenic structure at this mobile, exposed antigenic site and imply that intratypic antigenic variation of FMDV of serotype C is due to subtle structural differences that affect antibody recognition while preserving a functional structure for the receptor binding site.

Amino Acid Sequence↗
PubMed2005

VSG switching in Trypanosoma brucei: antigenic variation analysed using RNAi in the absence of immune selection.

Trypanosoma brucei relies on antigenic variation of its variant surface glycoprotein (VSG) coat for survival. We show that VSG switching can be efficiently studied in vitro using VSG RNAi in place of an immune system to select for switch variants. Contrary to models predicting an instant switch after inhibition of VSG synthesis, switching was not induced by VSG RNAi and occurred at a rate of 10(-4) per division. We find a highly reproducible hierarchy of VSG activation, which appears to be capable of resetting, whereby more than half of the switch events over 12 experiments were to one of two VSGs. We characterized switched clones according to switch mechanism using marker genes in the active VSG expression site (ES). Transcriptional switches between ESs were the preferred switching mechanism, whereby at least 10 of the 17 ESs identified in T. brucei 427 can be functionally active in vitro. We could specifically select for switches mediated by DNA rearrangements by inducing VSG RNAi in the presence of drug selection for the active ES. Most of the preferentially activated VSGs could be activated by multiple mechanisms. This VSG RNAi-based procedure provides a rapid and powerful means for analysing VSG switching in African trypanosomes entirely in vitro.

Animals↗
PubMed2006

Evaluation of antigenic variations between two virulent toxoplasma strains.

Toxoplasma gondii infection in humans is routinely assessed by serological means. Here, the authors attempted to compare the response of different Toxoplasma strains to serological tests and to evaluate the antigenic profiles of the RH and RH Ankara (TRH) strains with Western blotting. Anti-Toxoplasma IgG antibodies of 72 patients were examined with the indirect immunofluorescence antibody (IFA) test, ELISA and Western blotting (WB) by using antigen from both strains. Antigenic variations between strains did not affect IFA and ELISA test results, but qualitative and quantitative differences between the WB patterns were observed. A number of bands with molecular masses varying between 17 and 105 kDa were detected in WB. Fourteen different bands were obtained with the assay performed with RH strain antigen. An additional four bands were observed with TRH strain antigen. Also, an 80 kDa band was observed to stain darker in the blot with TRH strain antigen, whereas with RH strain antigen 30 and 38 kDa bands were darker. The results showed that strain-specific polymorphism in tachyzoite antigens of different Toxoplasma strains is important in the evaluation of WB but not in conventional serological analyses such as ELISA and IFA.

Animals↗
PubMed2001

Antigenic variation among equine H 3 N 8 influenza virus hemagglutinins.

To provide information on the antigenic variation of the hemagglutinins (HA) among equine H 3 influenza viruses, 26 strains isolated from horses in different areas in the world during the 1963-1996 period were analyzed using a panel of monoclonal antibodies recognizing at least 7 distinct epitopes on the H 3 HA molecule of the prototype strain A/equine/Miami/1/63 (H 3 N 8). The reactivity patterns of the virus strains with the panel indicate that antigenic drift of the HA has occurred with the year of isolation, but less extensively than that of human H 3 N 2 influenza virus isolates, and different antigenic variants co-circulate. To assess immunogenicity of the viruses, antisera from mice vaccinated with each of the 7 representative inactivated viruses were examined by neutralization and hemagglutination-inhibition tests. These results emphasize the importance of monitoring the antigenic drift in equine influenza virus strains and to introduce current isolates into vaccine. On the basis of the present results, equine influenza vaccine strain A/equine/Tokyo/2/71 (H 3 N 8) was replaced with A/equine/La Plata/1/93 (H 3 N 8) in 1996 in Japan. The present results of the antigenic analysis of the 26 strains supported the results of a phylogenetic analysis, that viruses belonging to each of the Eurasian and American equine influenza lineages have independently evolved. However, the current vaccine in Japan consists of two American H 3 N 8 strains; A/equine/Kentucky/1/81 and A/equine/La Plata/1/93. It is also therefore recommended that a representative Eurasian strain should be included as a replacement of A/equine/Kentucky/1/81.

Animals↗
PubMed2003

Regulation of antigenic variation in Plasmodium falciparum: censoring freedom of expression?

Plasmodium falciparum employs a strategy of clonal antigenic variation to evade the host immune response during the intraerythrocytic stage of its life cycle. The major variant parasite molecule is the P. falciparum erythrocyte membrane protein (PfEMP)1, which is encoded by the var multigene family. The parasite switches between different PfEMP1 molecules through regulation of var transcription. Recent studies have shed considerable light on this process, but much remains unknown. However, striking parallels between transcriptional control of var and genes in other organisms provide direction for future studies.

Animals↗
PubMed1985

Effect of 3-aminobenzamide on antigenic variation of Trypanosoma brucei.

African trypanosomes, like Trypanosoma brucei, depend on antigenic variation to evade the immune response of the vertebrate host. An antigenic switch corresponds to the activation of a variable surface glycoprotein (VSG) gene from a large silent repertoire. Most switches require the duplicative transposition of a VSG gene, which involves strand breaks in DNA and subsequent repair. The nuclear enzyme adenosine-diphosphoribosyl transferase (ADPRT), which is dependent on the presence of DNA strand breaks for its activity, might be involved in this process because it has a regulatory role in DNA repair in all eukaryotic cells studied so far. In previous work, the presence of ADPRT activity was demonstrated in T. brucei. Moreover, it was also shown in isolated trypanosomes the ADPRT activity, which is stimulated by the induction of DNA strand breaks, could be blocked by the competitive inhibitor 3-aminobenzamide. Here we report experiments using rats which were infected with small numbers of T. brucei expressing VSG gene 118. After two days, the rats were coupled to a continuous intraperitoneal infusion system administrating 3-aminobenzamide in 0.9% NaCl (81.4 mM) at a rate of 0.65 ml/hr/rat for a period of up to five days. Control rats received only a 0.9% NaCl infusion. At days 1, 3 and 5, 250 microliters blood was obtained from a tail artery. Plasma 3-aminobenzamide was determined using a new high performance liquid chromatography method, developed for these experiments. In most rats the plasma concentrations were maintained between 0.8 and 1.2 mM. The rate of antigenic switching was determined by quantitating the fraction of trypanosomes that had lost their VSG 118 coat, using antibody against VSG 118 and a limiting dilution in mice. The average switching rate found was 2.0 X 10(-6) in controls and 1.3 X 10(-7) in drug-treated rats (15-fold reduction). This suggests that ADPRT is required for completing most antigenic switching events. We discuss the possibility that drug-resistant switching only involves non-duplicative VSG gene activation.

Animals↗
PubMedDate not supplied

Antigenic variation of a major surface glycoprotein of Pneumocystis carinii.

The mannosylated surface glycoprotein (gp) of Pneumocystis carinii has one known conserved epitope that is recognized by the monoclonal antibody 85-1-5E12. The gp exhibits host species-specific antigenic variation, exhibits host species-specific collagenase sensitivity, and varies in size depending on the host of origin and the method of preparation. These data support the existence of host species-specific serotypes of P. carinii.

Animals↗
PubMed1980

Antigenic variation in trypanosomes: a computer analysis of variant order.

African trypanosomes can undergo antigenic variation and evade the host immune response. Whether the antigenic variants arise in an ordered sequence or randomly has been in dispute but has not been statistically tested. The coefficient of concordance (W), a statistic designed to detect similarities between sequences of objects, was applied to the literature data. The tendency towards a reproducible order of variants was strong, although in several of the studies the number of experimental animals was so low that no conclusions could be drawn. A computer model was used to determine whether this degree of order could arise with random generation of variants followed by selection. The model simulated a trypanosome clone with 90 possible variants, widely differing variant-specific growth rates, random variant origin and variant eradication by an anamnestic host immune response. Parameters varied were maximum parasitaemia, growth rate differential between 'fast' and 'slow' variants, and parasitologist ability to detect minor variants. Random generation and selection by growth rate alone could not produce the degree of variant orderliness reported in the literature. However, experiments with larger numbers of host animals and direct investigation of variant growth rates and competitive interactions are necessary before the random generation-selection hypothesis can be proven or disproven.

Analysis of Variance↗
PubMed1991

Mathematical biology of HIV infections: antigenic variation and diversity threshold.

Infection with the human immunodeficiency virus (HIV) results in severe damage to the immune system and consequent disease (AIDS) after a long and variable incubation period (on average 8-10 years). Why the incubation period should be so long is a puzzle. We outline an explanation based on the dynamics of the interplay between the immune response and antigenic variation in the virus population. The essential idea is that AIDS results when the diversity of antigenic variants of HIV in an infected patient exceeds some threshold, beyond which the immune system can no longer cope. The paper develops a simple mathematical model for this process, based on experimental observations, and explores several ramifications.

Acquired Immunodeficiency Syndrome↗
PubMed1980

An introduction to antigenic variation in trypanosomes.

The salivarian trypanosomes have a unique capacity for antigenic variation at the cell surface. This phenomenon is their primary mechanism for evasion of the host's immune response. Variation is mediated through alternate expression of an extensive repertoire of variant surface glycoproteins (VSGs). Extensive amino acid sequence diversity is responsible for the antigenic diversity of VSGs. All the isolated VSGs of Trypanosoma brucei studied also contain an immunologically cross-reacting glycosyl side chain at the C-terminus, which probably represents a recognition site for proteolytic processing of the hydrophobic putative membrane-binding tail present on the synthesized molecule but not so far found on purified VSGs.

Amino Acid Sequence↗
PubMed1988

Genomic rearrangements associated with antigenic variation in Campylobacter coli.

Campylobacter coli and Campylobacter jejuni share a limited number of highly conserved DNA sequences with members of the family Enterobacteriaceae. One of these sequences was cloned from C. coli VC167, and the region of homology to the enteric sequences was determined to be confined to a 700-base-pair region. The DNA represented in this clone undergoes a programmed, reversible rearrangement in VC167 that is associated with flagellar antigenic variation.

Antigenic Variation↗
PubMed1984

Antigenic variation in Trypanosoma vivax: isolation of a serodeme.

Studies of antigenic variation in Trypanosoma vivax have been hindered by its low infectivity to laboratory hosts and difficulties in obtaining defined cloned populations. The recent isolation of mouse-infective T. vivax has partially overcome the first problem. We have developed a highly efficient cloning technique which has been applied to the isolation of a collection of 71 clones, representing 31 distinct variable antigen types, of mouse-infective T. vivax from Nigeria. This serodeme showed no cross-reaction with several T. brucei-group serodemes, but some cross-reaction with naturally occurring Kenyan T. vivax.

Animals↗
PubMed1983

DNA rearrangements and antigenic variation in Trypanosoma equiperdum: multiple expression-linked sites in independent isolates of trypanosomes expressing the same antigen.

African trypanosomes resist the immune response of their mammalian hosts by varying the surface glycoprotein which constitutes their antigenic identity. The molecular mechanism of this antigenic variation involves the successive activation of a series of genes which code for different variant surface glycoproteins (VSGs). We have studied the expression of two VSG genes (those of VSG-1 and VSG-28) in Trypanosoma equiperdum, and we report the following findings. (i) The expression of both VSG genes is associated with the duplication and transposition of corresponding basic copy genes. (ii) The duplicated transposed copy appears to be the expressed copy. (iii) Although there are multiple genes which cross-hybridize with the VSG-1 cDNA probe, only one of these appears to be used as a template for the expression-linked copy in four independent BoTat-1 clones. (iv) Analysis of the genomic environments of the expressed VSG-1 genes from each of four independently derived BoTat-1 trypanosome clones revealed that there are at least three different sites into which the expression-linked copy can be inserted.

Animals↗
PubMed2006

Antigenic variation in Babesia bovis occurs through segmental gene conversion of the ves multigene family, within a bidirectional locus of active transcription.

Antigenic variation in Babesia bovis is one aspect of a multifunctional virulence/survival mechanism mediated by the heterodimeric variant erythrocyte surface antigen 1 (VESA1) protein that also involves endothelial cytoadhesion with sequestration of mature parasitized erythrocytes. The ves1alpha gene encoding the VESA1a subunit was previously identified. In this study, we present the unique organization of the genomic locus from which ves1alpha is transcribed, and identify a novel branch of the ves multigene family, ves1beta. These genes are found together, closely juxtaposed and divergently oriented, at the locus of active transcription. We provide compelling evidence that variation of both transcriptionally active genes occurs through a mechanism of segmental gene conversion involving sequence donor genes of similar organization. These results also suggest the possibility of epigenetic regulation through in situ switching among gene loci, further expanding the potential repertoire of variant proteins.

Amino Acid Sequence↗
PubMed1980

Studies on Trypanosoma (nannomonas) congolense III. Antigenic variation in three cyclically transmitted stocks.

Cyclical transmission of different variable antigen types of Trypanosoma congolense STIB 228 resulted in the development of metacyclic trypanosome populations which were similar in their variable antigen composition as judged by immunofluorescence and neutralization assays. The variable antigen types present in the ingested bloodstream populations were not found in the metacyclic populations. The bloodstream populations which were obtained from cyclically infected, irradiated (900 rad.) mice contained variable antigen types which were not present in the corresponding metacyclic populations. When derivatives of 2 other stocks of T. congolense, isolated in different area of Tanzania, underwent cyclical development in the tsetse fly, the metacyclic populations of each stock also had a characteristic variable antigen composition. The metacyclic populations of the 3 stocks were, however, completely dissimilar in variable antigen composition. Simultaneous infection of tsetse flies with a mixture of different stocks resulted in the concurrent production of metacyclic trypanosomes which contained the characteristic variable antigen types of each stock. The effect of cyclical transmission on the process of antigenic variation in T. congolense infections is therefore similar to that in T. brucei infections.

Animals↗