Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Antigenic Variation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1997

Antigenic variation in Foot and Mouth Disease Virus type Asia 1 isolates circulated during 1993-95 in India.

The antigenic variation in Foot and Mouth Disease Virus (FMDV) is very high. The effective strategy to control the Foot and Mouth Disease (FMD) in India which is a habitat of four serotypes O, A, C and Asia 1, is by regular vaccination, using the vaccine strain most suitable for the local situation. India is an endemic country with the disease being widely distributed. Selection of vaccine strain should therefore need the information on the circulating viruses. Asia 1 causes the second largest number of disease outbreaks in India. As there is no information available with respect to the extent of antigenic variation in FMDV type Asia 1, we have studied FMDV isolates from vaccinated and unvaccinated animals from different parts of the country and compared their relationship with Asia 1 vaccine virus. The immunogenic, hypervariable region of viral protein 1 (VP1) gene was amplified by RT-PCR and sequenced. Analysis of sequence data showed that the viruses from two field outbreaks of Southern India were closely related to each other when compared to the isolate from the North and all the three isolates are away from the vaccine virus.

Animals↗
PubMed1985

Antigenic variation in Trypanosoma evansi: variable antigen type (VAT) composition of first relapse populations in mice.

The variable antigen type (VAT) composition of first relapse populations developing in mice infected with 11 VAT populations of a stock of T. evansi was shown to be independent of the infecting VAT. Trypanosomes representing three of the VATs were found in all relapse populations resulting from infection with each VAT. A further seven VATs were detected in at least one relapse population from each VAT. These 10 VATs had previously been classed as predominant VATs from studies on VAT development in rabbits, sheep and goats. It is probable, therefore, that the VAT composition of first relapse populations can be used as a basis for the classification of T. evansi stocks into serodemes according to their predominant VAT repertoires.

Animals↗
PubMed1985

Antigenic variation in the hemagglutinin-neuraminidase protein of human parainfluenza type 3 virus.

Sixteen monoclonal antibodies directed to the hemagglutinin-neuraminidase (HN) protein of a 1957 isolate of parainfluenza type 3 virus (PIV3) were produced and used to examine antigenic variation in clinical strains. Analysis of hemagglutination-inhibition reactivity patterns of antigenic variants selected in vitro in the presence of monoclonal antibodies indicated that there were a minimum of six distinct epitopes detectable on the HN molecule. Competitive-binding assays indicated that these epitopes were located in two topologically nonoverlapping antigenic sites. An additional four epitopes were detected when 37 PIV3 clinical strains isolated over a period of 26 years in three geographic regions were tested for reactivity with the antibodies. Of the 10 unique epitopes defined by our monoclonal antibodies, 5 did not undergo detectable antigenic variation in any of the 37 strains examined. These results were expected since PIV3 viruses have been characterized as being antigenically monotypic. In contrast, antigenic variation was detected in the remaining five epitopes. This variation was not characterized by the accumulation of antigenic alterations with time (as for influenza A viruses), but appeared to represent genetic heterogeneity within the PIV3 population.

Animals↗
PubMedDate not supplied

Antigenic variation in vector-borne pathogens.

Several pathogens of humans and domestic animals depend on hematophagous arthropods to transmit them from one vertebrate reservoir host to another and maintain them in an environment. These pathogens use antigenic variation to prolong their circulation in the blood and thus increase the likelihood of transmission. By convergent evolution, bacterial and protozoal vector-borne pathogens have acquired similar genetic mechanisms for successful antigenic variation. Borrelia spp. and Anaplasma marginale (among bacteria) and African trypanosomes, Plasmodium falciparum, and Babesia bovis (among parasites) are examples of pathogens using these mechanisms. Antigenic variation poses a challenge in the development of vaccines against vector-borne pathogens.

Anaplasma↗
PubMed1985

Neutralization kinetic analysis of echovirus 30 and coxsackievirus B4 strains revealed little antigenic variation amongst the echovirus strains.

An antigenic analysis was made of echovirus 30 and coxsackievirus B4 isolates by determining neutralization rate constants in neutralization kinetic tests. The seven echovirus 30 isolates included the prototype strain and six others isolated in Melbourne, Australia, between 1959 and 1982. Little antigenic heterogeneity was observed in contrast to the evidence of antigenic variation recorded in similar tests on seven coxsackievirus B4 isolates. These isolates also included the prototype strain, as well as six others isolated in Melbourne between 1958 and 1973. The results obtained with the coxsackievirus B4 isolates were in keeping with those observed particularly with the polioviruses and also coxsackievirus B4 by other workers. Those obtained with the echovirus 30 isolates were unexpected, as this virus is also a member of the enterovirus group.

Antigens, Viral↗
PubMed1990

Antigenic variation of Giardia lamblia in the feces of Mongolian gerbils.

Enzyme-linked immunoelectrotransfer blot was used to study variations in Giardia lamblia antigens in extracts of feces from infected Mongolian gerbils. A 65-kilodalton antigen was found in feces that contained strain WB (ATCC 30957) cysts and in axenic culture of strains WB and CDC:0284:1 that contained trophozoites. The 65-kilodalton antigen from trophozoites of both strains was membrane associated. A 70-kilodalton antigen was found in feces that contained strain CDC:0284:1 cysts. It was persistent in 16 fecal collections and may be strain specific. Similar variations in antigens may occur in human feces. Coproimmunodiagnostic assays that use monoclonal antibodies will have to include all varieties of G. lamblia antigens present in the feces of giardiasis patients.

Animals↗
PubMed2005

Telomeric heterochromatin propagation and histone acetylation control mutually exclusive expression of antigenic variation genes in malaria parasites.

Malaria parasites use antigenic variation to avoid immune clearance and increase the duration of infection in the human host. Variation at the surface of P. falciparum-infected erythrocytes is mediated by the differential control of a family of surface antigens encoded by var genes. Switching of var gene expression occurs in situ, mostly from telomere-associated loci, without detectable DNA alterations, suggesting that it is controlled by chromatin structure. We have identified chromatin modifications at telomeres that spread far into telomere-proximal regions, including var gene loci (>50 kb). One type of modification is mediated by a protein homologous to yeast Sir2 called PfSir2, which forms a chromosomal gradient of heterochromatin structure and histone hypoacetylation. Upon activation of a specific telomere-associated var gene, PfSir2 is removed from the promoter region and acetylation of histone occurs. Our data demonstrate that mutually exclusive transcription of var genes is linked to the dynamic remodeling of chromatin.

Animals↗
PubMed1997

The rate of antigenic variation in fly-transmitted and syringe-passaged infections of Trypanosoma brucei.

Rates of antigenic variation were measured in vivo in several populations of cloned lines of Trypanosoma brucei before and after cyclical transmission through tsetse flies. Two cloned lines were adapted for use in laboratory conditions by extensive syringe passaging and rates of antigenic switching/cell/generation were less than 3 x 10(-6) and 1 x 10(-4) in each line. Rates of switching were then determined after fly transmission of the first line and generated per capita rate values of greater than 2 x 10(-3) in three of four populations examined. In the fourth population the switch rate was lower: less than 7 x 10(-5) switches/ cell/generation. These data show that rates of antigenic variation are several orders of magnitude lower in syringe-passaged lines, such as those routinely used in the majority of laboratory studies, compared with most recently fly-transmitted lines. They also show that the reduction in switching rate associated with syringe passaging is reversible and is thus unlikely to be caused by mutation.

Animals↗
PubMed1993

Antigenic variation of pilin regulates adhesion of Neisseria meningitidis to human epithelial cells.

Pili have been shown to play an essential role in the adhesion of Neisseria meningitidis to epithelial cells. However, among piliated strains, both inter- and intrastrain variability exist with respect to their degree of adhesion to epithelial cells in vitro (Virji et al., 1992). This suggests that factors other than the presence of pili per se are involved in this process. The N. meningitidis pilin subunit undergoes extensive antigenic variation. Piliated low- and high-adhesive derivatives of the same N. meningitidis strain were selected and the nucleotide sequence of the pilin gene expressed in each was determined. The highly adhesive derivatives had the same pilin sequence. The alleles encoding the pilin subunit of the low-adhesive derivatives were completely different from the one found in the high-adhesive isolates. Using polyclonal antibodies raised against one hyperadhesive variant, it was confirmed that the low-adhesive piliated derivatives expressed pilin variants antigenically different from the highly adhesive strains. The role of antigenic variation in the adhesive process of N. meningitidis was confirmed by performing allelic exchanges of the pilE locus between low- and high-adhesive isolates. Antigenic variation has been considered a means by which virulent bacteria evade the host immune system. This work provides genetic proof that a bacterial pathogen, N. meningitidis, can use antigenic variation to modulate their degree of virulence.

Amino Acid Sequence↗
PubMed1995

Genetic basis of Neisseria gonorrhoeae lipooligosaccharide antigenic variation.

Neisseria gonorrhoeae lipooligosaccharide (LOS) undergoes antigenic variation at a high rate, and this variation can be monitored by changes in a strain's ability to bind LOS-specific monoclonal antibodies. We report here the cloning and identification of a gene, lsi-2, that can mediate this variation. The DNA sequence of lsi-2 has been determined for N. gonorrhoeae 1291, a strain that expresses a high-molecular-mass LOS, and a derivative of this strain, RS132L, that produces a truncated LOS. In the parental strain, lsi-2 contains a string of 12 guanines in the middle of its coding sequence. In cells that had antigenically varied to produce a truncated LOS, the number of guanines in lsi-2 was altered. Site-specific deletions were constructed to verify that expression of a 3.6-kDa LOS is due to alterations in lsi-2.

Antigens, Bacterial↗
PubMed1991

Molecular biology of antigenic variation in Lyme borreliosis and relapsing fever: a comparative analysis.

Lyme borreliosis and relapsing fever are human diseases caused by different members of the genus Borrelia. Antigenic variation has been a well-known feature of the pathogenesis of relapsing fever for decades. More recently it has been recognized that Borrelia burgdorferi, the agent of Lyme borreliosis, also can vary its surface antigens. In this review the biology and molecular biology of antigenic variation of the pathogens in these two disorders are compared.

Antigenic Variation↗
PubMed2004

Antigenic variation in Trypanosoma brucei: facts, challenges and mysteries.

Antigenic variation allows African trypanosomes to develop chronic infections in mammalian hosts. This process results from the alternative occurrence of transcriptional switching and DNA recombination targeted to a telomeric locus that contains the gene of the variant antigen and is subjected to mono-allelic expression control. So far, the identification of mechanisms and factors involved still resists technological developments and genome sequencing.

Animals↗
PubMed1987

Antigenic variation of cloned Plasmodium fragile in its natural host Macaca sinica. Sequential appearance of successive variant antigenic types.

The course of infection of Plasmodium fragile in its natural host, the toque monkey Macaca sinica, consists of a primary peak of parasitemia followed by several distinct, successive peaks of lower parasitemia. In the S+ host, the late intraerythrocytic asexual developmental stages of P. fragile induce the expression of antigens on the surface of infected erythrocytes, which could be detected using the technique of surface immunofluorescence. Immunofluorescence using unfixed erythrocytes in suspension has shown that antigens are recognized by immune serum on the surface of the erythrocytes infected with more mature stages of the parasite. These antigens undergo variation, each successive peak of parasitemia being characterized by a different variant antigenic type (VAT). The appearance of the successive VATs occurs in a sequential manner, following the same order in different sets of animals. This constitutes the first example of a sequential expression of antigens in a malaria parasite; it indicates that, in P. fragile, antigenic variation is not the result of random mutations selected by antibody. Parasite-induced antigens on the surface of infected erythrocytes could not be detected in the S- host. However, when nonexpressing parasites from the S- host were transferred by blood passage into a naive S+ animal, they began to express antigens on the surface of infected erythrocytes within two erythrocytic cycles. We have demonstrated that the ability of S- parasites to switch to a particular VAT when passaged into a S+ animal changes during the course of an infection in the S- animal, indicating that, although surface antigens are not expressed, the processes leading to antigenic variation occurs even in the S- host. Antibodies directed against these surface antigens inhibit the growth of intra-erythrocytic parasites. The growth inhibition effects of antibodies are also variant specific, indicating that these variant surface antigens are functionally important for parasite survival.

Animals↗
PubMed1991

Antigenic variation of cytomegalovirus isolates recovered from infected children.

The present work investigated antigenic variations of the most immunogenic polypeptides of Cytomegalovirus (CMV), namely two nonstructural polypeptides of MW 72 Kd and 52 Kd, and 5 structural proteins of MW 150, 65, 58, 38 and 28 Kd, in several low-passage CMV isolates from urine of infected children. The polypeptides showing the greatest variations were the non structural p72 and p52, and the structural proteins p65 and p38. Furthermore the reactivity of the children's sera was studied with regard to the antigenic proteins of the homologous virus strain. We failed to recognize any reactivity pattern typical of an acute CMV infection and the results obtained indicate that CMV-infected children may have a very low and variable IgG and IgM response, p150 and p65 being the two most often recognized antigens.

Antibodies, Monoclonal↗
PubMed1994

Activation of a vmp pseudogene in Borrelia hermsii: an alternate mechanism of antigenic variation during relapsing fever.

The relapsing fever agent, Borrelia hermsii, undergoes multiphasic antigenic variation to evade its host's immune response. A frequently observed switch is serotype 7 to 26. Unlike silent vmp genes previously characterized, the transcriptionally silent vmp26 sequence was a pseudogene in lacking a start codon. In serotype 7 the location of the silent vmp26 sequence just downstream of vmp7 on the expression plasmid, as well as on the silent plasmid, was also unique. The demonstration of a predicted circular recombination product in serotype 7 but not serotype 21 populations indicates that the pseudogene was activated by an intramolecular recombination producing a deletion of DNA between 20-nucleotide direct repeats in vmp7 and psi vmp26.

Amino Acid Sequence↗
PubMed1982

Host parasite relationships in Trypanosoma (duttonella) vivax with special reference to the influence of antigenic variation.

A mouse model system was used to study various aspects of host and parasite relationships in Trypanosoma vivax infections. These included the phenomenon of antigenic variation, the variable parasite antigens responsible for this phenomenon, parasite-host adaption, host immune responses and the role of genes in the major histocompatibility complex in the control of infection. While the mouse model system has allowed investigation of these aspects of host parasite relationships, it is clear that the system is much more limited than those generally used in T. brucei spp and T. congolense infections. This is indicated by the discovery that not all VATs of T. vivax were equally infective for mice, though in some cases infectivity could be improved by bovine serum supplementation and/or immunosuppression of the mouse host. In the case of rats, infection was even restricted to a smaller number of the VATs studied. It was, however, possible to biochemically characterize the variable surface antigen carried by T. vivax and show its similarity to those carried by T. brucei and T. congolense. The H-2 complex was found not to influence acquired resistance of inbred strains. Cyclic transmissions of T. vivax infections to goats combined with chemotherapy were carried out in an attempt to induce protection to subsequent infection as has been shown in T. brucei and T. congolense infections. Such protection could, however, not be obtained, The failure of the metacyclic VATs to induce immunity, was perhaps due to rapid decrease in antibody titres to bloodstream VATs found after treatment and prior to rechallenge. The usefulness of the mouse model system in elucidating the mechanisms responsible for the non-H-2 linked differences in susceptibility to T. vivax infections should be further explored and its relevance to mechanisms of trypanotolerance in domestic ruminants defined.

Animals↗
PubMed2006

Antigenic variation by Borrelia hermsii occurs through recombination between extragenic repetitive elements on linear plasmids.

The relapsing fever agent Borrelia hermsii undergoes multiphasic antigenic variation through gene conversion of a unique expression site on a linear plasmid by an archived variable antigen gene. To further characterize this mechanism we assessed the repertoire and organization of archived variable antigen genes by sequencing approximately 85% of plasmids bearing these genes. Most archived genes shared with the expressed gene a <or= 62 nucleotide (nt) region, the upstream homology sequence (UHS), that surrounded the start codon. The 59 archived variable antigen genes were arrayed in clusters with 13 repetitive, 214 nt long downstream homology sequence (DHS) elements distributed among them. A fourteenth DHS element was downstream of the expression locus. Informative nucleotide polymorphisms in UHS regions and DHS elements were applied to the analysis of the expression site of relapse serotypes from 60 infected mice in a prospective study. For most recombinations, the upstream crossover occurred in the UHS's second half, and the downstream crossover was in the DHS's second half. Usually the closest archival DHS element was used, but occasionally a more distant DHS was employed. The downstream extragenic crossover site in B. hermsii contrasts with the upstream [corrected] extragenic crossover site for antigenic variation in African trypanosomes.

Antigenic Variation↗
PubMed2005

Distinct roles for two RAD51-related genes in Trypanosoma brucei antigenic variation.

In Trypanosoma brucei, DNA recombination is crucial in antigenic variation, a strategy for evading the mammalian host immune system found in a wide variety of pathogens. T.brucei has the capacity to encode >1000 antigenically distinct variant surface glycoproteins (VSGs). By ensuring that only one VSG is expressed on the cell surface at one time, and by periodically switching the VSG gene that is expressed, T.brucei can evade immune killing for prolonged periods. Much of VSG switching appears to rely on a widely conserved DNA repair pathway called homologous recombination, driven by RAD51. Here, we demonstrate that T.brucei encodes a further five RAD51-related proteins, more than has been identified in other single-celled eukaryotes to date. We have investigated the roles of two of the RAD51-related proteins in T.brucei, and show that they contribute to DNA repair, homologous recombination and RAD51 function in the cell. Surprisingly, however, only one of the two proteins contributes to VSG switching, suggesting that the family of diverged RAD51 proteins present in T.brucei have assumed specialized functions in homologous recombination, analogous to related proteins in metazoan eukaryotes.

Amino Acid Sequence↗