Genetic variation in host susceptibility to attack by the mahogany shoot borer, Hypsipyla grandella (Zeller)

1999 ◽  
Vol 1 (1) ◽  
pp. 11-18 ◽  
Author(s):  
A. C. Newton ◽  
A. D. Watt ◽  
F. Lopez ◽  
J. P. Cornelius ◽  
J. F. Mesén ◽  
...  
Parasitology ◽  
1985 ◽  
Vol 90 (1) ◽  
pp. 205-216 ◽  
Author(s):  
D. J. Minchella

Over half of all living species of plants and animals are parasitic, which by definition involves intimate association with and unfavourable impact on hosts (Price, 1980). This paper will only consider parasites whose ‘unfavourable impact’ adversely affects the birth and/or mortality rates of their hosts (Anderson, 1978). Most organisms are potential hosts and must deal with the problem of parasitism. The probability of parasitic infection of a host is influenced by both environmental and genetic factors. Traditionally it was assumed that a host was either resistant or susceptible to a particular parasite and therefore the interaction between a parasite and potential host had only two possible outcomes: either the resistant host rebuffed the parasitic attack and remained uninfected or the parasite successfully invaded and significantly reduced the reproductive success of the susceptible host. This approach, however, ignored the intraspecific genetic variation present within both host and parasite populations (Wakelin, 1978). Since the outcome is determined by the interaction of a finite set of host genes and parasite genes, genetic variation in host susceptibility and parasite infectivity (Richards, 1976; Wakelin, 1978) suggests that more than two outcomes are possible. Variation in host and parasite genomes does not begin and end at the susceptibility/infectivity loci. Other genes may also influence the outcome of host–parasite interactions by altering the life-history patterns of hosts and parasites, and lead to a variety of outcomes.


2018 ◽  
Author(s):  
Elizabeth ML Duxbury ◽  
Jonathan P Day ◽  
Davide Maria Vespasiani ◽  
Yannik Thüringer ◽  
Ignacio Tolosana ◽  
...  

AbstractIt is common to find considerable genetic variation in susceptibility to infection in natural populations. We have investigated whether natural selection increases this variation by testing whether host populations show more genetic variation in susceptibility to pathogens that they naturally encounter than novel pathogens. In a large cross-infection experiment involving four species of Drosophila and four host-specific viruses, we always found greater genetic variation in susceptibility to viruses that had coevolved with their host. We went on to examine the genetic architecture of resistance in one host species, finding that there are more major-effect genetic variants in coevolved host-parasite interactions. We conclude that selection by pathogens increases genetic variation in host susceptibility, and much of this effect is caused by the occurrence of major-effect resistance polymorphisms within populations.


2019 ◽  
Vol 16 (4) ◽  
pp. 297-301
Author(s):  
Khurshid Iqbal ◽  
Muhammad Imran ◽  
Shafi Ullah ◽  
Muhsin Jamal ◽  
Yasir Waheed

Background: Human immunodeficiency virus (HIV) infection is a global health burden which ultimately results in acquired immune deficiency syndrome (AIDS). There are multiple host factors which are capable of limiting HIV-1 replication. One of the most important host factors which inhibit HIV-1 DNA synthesis is the apolipoprotein B mRNA-editing enzyme, catalytic polypeptide- like 3G (APOBEC3G). Any genetic variation of this important host factor may influence the host susceptibility to viral infection. Objective: The aim of the current study was to evaluate any correlation of APOBEC3G genetic variation rs8177832 with HIV-1 infection. Methods: The study involved 142 healthy control and 100 HIV-1 infected subjects. The genetic variation rs8177832 of all studied subjects was determined by allele-specific polymerase chain reaction (AS-PCR). Results: The results showed that the distribution of rs8177832 genotypes AA, AG and GG in healthy subjects and HIV-1 subjects was; 42.253%, 42.957%, 14.788% and 66%, 27%, 7% respectively. Statistical analyses of data showed that there was a significant variation in rs8177832 genotype AA in healthy control and HIV-1 infected subjects (42.257% vs 66%; p-value<0.001). Conclusion: Thus it was concluded that APOBEC3G rs8177832 AA genotype contributes in genetic predisposition to HIV-1 infection in Pakistani population.


2010 ◽  
Vol 277 (1695) ◽  
pp. 2737-2745 ◽  
Author(s):  
A. R. Allen ◽  
G. Minozzi ◽  
E. J. Glass ◽  
R. A. Skuce ◽  
S. W. J. McDowell ◽  
...  

The prevalence of bovine tuberculosis (BTB) in the UK remains a significant economic burden and problem for the agri-food industry. Much effort has been directed towards improving diagnostics, finding vaccine candidates and assessing the usefulness of badger culling. The contribution that host genotype makes to disease outcome has, until recently, been overlooked; yet, it is biologically untenable that genetic variation does not play a role. In this review, we highlight the evidence, past and present, for a role of host genetics in determining susceptibility to BTB in livestock. We then address some of the major issues surrounding the design of future studies tasked with finding the exact causative genetic variation underpinning the TB susceptibility phenotype. Finally, we discuss some of the potential future benefits, and problems, that a knowledge of the genetic component to BTB resistance/susceptibility may bring to the agricultural industries and the wider scientific community.


1973 ◽  
Vol 3 (4) ◽  
pp. 585-589 ◽  
Author(s):  
K. Illingworth

Sirococcusstrobilinus Preuss. was identified as the cause of a shoot blight of lodgepole pine (Pinuscontorta Dougl. ex Loud.) seedlings grown in a nursery in central British Columbia. Marked variation in susceptibility to this fungus was noted among the 153 provenances representing the entire range of lodgepole pine. Genetic variation in host susceptibility is inferred.


2021 ◽  
Author(s):  
Aparajita Singh ◽  
Aabeer Basu ◽  
Biswajit Shit ◽  
Tejashwini Hegde ◽  
Nitin Bansal ◽  
...  

The host susceptibility to one pathogen can decrease, increase, or remain unaffected by virtue of the host evolving resistance towards a second pathogen. Negative correlations between a host susceptibility to different pathogens is an often-cited explanation for maintenance of genetic variation in immune function determining traits in a host population. In this study, we investigated the change in susceptibility of Drosophila melanogaster flies to various novel bacterial pathogens after being experimentally selected for increased resistance to one particular bacterial pathogen. We independently selected flies to become more resistant towards Enterococcus faecalis and Pseudomonas entomophila, and baring a few exceptions the evolved populations exhibited cross-resistance against the range of pathogens tested in the study. Neither the identity of the native pathogen nor the host sex was major determining factors in predicting the pattern of cross-resistance exhibited by the selected populations. We therefore report that a generalized cross-resistance to novel pathogens can repeatedly evolve in response to selection for resistance against a single pathogen.


2019 ◽  
Vol 13 (1) ◽  
pp. 48-61 ◽  
Author(s):  
Catherine I. Cullingham ◽  
Rhiannon M. Peery ◽  
Colleen E. Fortier ◽  
Elizabeth L. Mahon ◽  
Janice E. K. Cooke ◽  
...  

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yulong Chen ◽  
Xunjun Yang ◽  
Yao Chen ◽  
Guorong Chen ◽  
Cheryl A. Winkler ◽  
...  

Abstract Background Hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) remains a major public health problem and its pathogenesis remains unresolved. A recent proteomics study discovered a lipid enzyme Sterol O-acyltransferase (SOAT1) involvement in the progression of HCC. We aimed to explore the association between SOAT1 genetic variation and HCC. Methods We genotyped three exonic SOAT1 variants (rs10753191, V323V; rs3753526, L475L; rs13306731, Q526R) tagging most variations in the gene, in 221 HCC patients and 229 healthy individuals, to assess the impact of SOAT1 gene variation on risk of HCC occurrence. We further conducted immunohistochemistry to compare SOAT1 protein expression levels in 42 paired tumor and adjacent non-tumor tissues. Results We found that rs10753191 (Odds ratio (OR) = 0.58, P = 0.04) and a haplotype TGA (OR = 0.40, P = 0.01) were associated with reduced HCC risk after adjusting for lipid levels. In the immunohistochemistry experiment, we found that the protein expression of SOAT1 was significantly increased in the tumor compared with adjacent tissue (P < 0.001). Conclusion This study revealed for the first time SOAT1 genetic variation that associates with host susceptibility to HCC occurrence. Our results suggest a role of SOAT1 in the HCC development, which warrants further elucidation.


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