How can comparative genomics assist in the treatment of HIV? Understanding the evolution of HIV in an individual will help scientist understand how the virus responds to different drug regimes and will lead to better treatments. 10 The human genome project led to the discovery that much of the genome consists of repeated sequences of nucleotides.
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What is comparative genomics?
Comparative Genomics: Volumes 1 and 2. Totowa (NJ): Humana Press; 2007. Comparative Genomics: Volumes 1 and 2. Show details ... For a detailed treatment of the theory of alignment ... Hermankova et al. studied the HIV-1 drug resistance profiles in children and adults receiving combination drug therapy. To identify the SNPs in the HIV-1 isolates ...
Can HIV gene therapy be used to treat HIV?
Mar 21, 2022 · As previously described, HIV-1 sequence assembly was performed by our in-house pipeline (Defective and Intact HIV Genome Assembler), which is capable of reconstructing thousands of HIV genomes within hours via the assembly of raw sequencing reads into annotated HIV genomes . The steps executed by the pipeline are described briefly as follows.
What is the first step in comparative genomics?
Jan 31, 2013 · A complete human gene set and DNA sequence was available to help combat the more inscrutable deadly chronic and infectious diseases , and this has enabled the investigation of HIV/AIDS using the new tools of genomics. AIDS exhibits abundant epidemiological heterogeneity, much of which could be attributed to host genetic factors.
What is the best approach to cure HIV?
The history of HIV gene therapy is especially intriguing, in that the virus that was targeted was soon co-opted to become part of the targeting strategy. Today, HIV-based lentiviral vectors, along with many other gene delivery strategies, have been used to evaluate HIV cure approaches in cell culture, small and large animal models, and in patients.
Which of the following are benefits of sequencing the human genome?
The primary purpose of sequencing one's genome is to obtain information of medical value for future care. Genomic sequencing can provide information on genetic variants that can lead to disease or can increase the risk of disease development, even in asymptomatic people.
Which of the following term applies to the study of all the proteins produced by an organism?
Proteomics is the large-scale study of proteomes. A proteome is a set of proteins produced in an organism, system, or biological context.
What are the benefits of sequencing the human genome quizlet?
It helps to connect the biology of model organisms to human physiology. What do comparative genomic studies help us? They can decipher the roles of protein coding genes, noncoding RNAs, and regulatory sequences in evolution.
Why has str become the method of choice over DNA fingerprinting?
Why has STR become the method of choice over DNA fingerprinting when identifying a person of interest? STR doesn't require the use of restriction enzymes. In producing transgenic plants, cells called protoplasts are often used. Protoplasts are plant cells from which the cell wall has been removed.
What is the relationship between genome and proteome of a system?
Within an individual organism, the genome is constant, but the proteome varies and is dynamic. Every cell in an individual organism has the same set of genes, but the set of proteins produced in different tissues differ from one another and are dependent on gene expression.
What is the relationship between genome and proteome?
The proteome is an expression of an organism's genome. However, in contrast with the genome, which is characterized by its stability, the proteome actively changes in response to various factors, including the organism's developmental stage and both internal and external conditions.
What is one benefit of mapping the human genome?
Genetic mapping - also called linkage mapping - can offer firm evidence that a disease transmitted from parent to child is linked to one or more genes. Mapping also provides clues about which chromosome contains the gene and precisely where the gene lies on that chromosome.Aug 17, 2020
Why was sequencing the human genome so beneficial to the study of human genetics and the genetics of other species?
Why study our genome? Working out the sequence of the base pairs in all our genes enables us to understand the code that makes us who we are. This knowledge can then give us clues on how we develop as embryos, why humans have more brainpower than other animals and plants, and what happens in the body to cause cancer.May 14, 2015
What is the goal of functional genomics?
The goal of functional genomics is to provide a comprehensive, annotated map of the downstream effects of all coding and non-coding parts of the genome.
How does STR testing work?
As the name implies, short tandem repeat (STR) analysis is a method of determining an individual's DNA profile by counting the number of times a small DNA sequence (short tandem repeat unit) is repeated at a specific chromosomal location.
How accurate is STR analysis?
Typically each STR allele will be shared by around 5 - 20% of individuals. The power of STR analysis comes from looking at multiple STR loci simultaneously[6]. The pattern of alleles can identify an individual quite accurately. Thus STR analysis provides an excellent identification tool.
How are DNA fingerprints and restriction maps similar different explain?
How are DNA fingerprints and restriction maps similar? Explain. A restriction map is a map of known restriction sites within a sequence of DNA. These might be like a fingerprint because fingerprints are judged by certain points as well and the shapes at those points determine who the print belongs to.
What is a GWAS in HIV?
Unlike association studies of candidate genes, GWAS scan the entire genome with hundreds of thousands (if not millions) of common human SNPs to discover genome regions that statistically associate with explicit AIDS endpoints in large cohort studies (Box 1 ). Fellay et al. [ 11] reported the first AIDS GWAS in 2007. Their study tracked the HIV set point (mean plasma viral RNA level over several months once the immune system has settled to a steady state level after initial spikes in virus upon HIV infection; see Box 1) in 486 European AIDS patients from the Euro-Center for HIV/AIDS Vaccine Immunology (CHAVI) cohort that were genotyped with an Illumina 550,000 SNP array. Fellay et al. discovered three genome-wide significant (after Bonferroni correction for multiple SNP tests; <9.3 × 10 -8) SNPs nested within the HLA complex, including a proxy-SNP in linkage disequilibrium (LD) HLA-B*5701, a known protective influence on AIDS progression. Since then ten additional GWAS using different cohorts, and different AIDS stages (phenotypes), arrays and numbers of SNPs, have appeared [ 32 – 41 ]. The combined GWAS have consistently fingered HLA SNPs, but agreed on little else.
Why was the PARD3B study limited to a single endpoint?
The PARD3B study was intentionally limited to a single endpoint or phenotype (time of progression as defined by the AIDS 1987 Centers for Disease Control) to avoid statistical penalties for multiple tests. Yet many different gene association tests are possible with the rich clinical and genetic data we have collected across the years on these retrospective AIDS cohorts; indeed, many of these tests were performed and considered supportive in the previous candidate gene studies [ 7, 10] (Table 1 ). In spite of the aversion to multiple test statistical correction penalties, there is information than can be gleaned from detailed clinical data that should be explored. Hutcheson et al. [ 7] described useful heat plots that allow one to inspect the pattern of genetic association across many tests, as well as across small regions of the genome in strong LD. The combination of multiple non-independent statistical signals is a challenge to interpret, but in cases of known genes, such as CCR5-Δ32, HLA and IL10, the patterns are illuminating. The heat plots also provide a derivative approach to public data sharing of GWAS results without the problem of violating the informed consent and privacy constraints set out by Institutional Review Boards, which often restrict open access to human cohort data [ 46 ]. For example, posting an unabridged table of GWAS results online (odds ratios, P -values and confidence intervals), together with two-dimensional and three-dimensional visualization heat plots, would allow researchers to freely inspect the results of a published GWAS [ 40 ], in any genomic region they may discover in a different cohort, for independent replication purposes - without viewing patients' confidential clinical or genotypic information.
What is CCR5-32 mutation?
The first and perhaps most provocative ARG involved the description of CCR5-Δ32, a 32 base pair deletion frameshift mutation that truncates C-C chemokine receptor 5 (CCR5), the HIV entry receptor on lymphoid cells [ 12 – 14] (see Box 2 for a discussion of the origin of this mutation). Epidemiological studies showed that individuals homozygous for CCR5-Δ32 had a 100-fold reduction in HIV infection incidence: the genotype seems to confer near complete protection from HIV infection (Figure 1 ). Individuals in large cohort studies that are heterozygous for CCR5-Δ32, although susceptible to infection, consistently have a delayed onset of AIDS by two to four years, likely due to the diminishing onset of B-cell lymphoma [ 12, 15 ]. Further, AIDS patients on HAART live longer when they are heterozygous for the CCR5-Δ32 mutation, due to faster HIV viral load suppression, and progress to AIDS more slowly than CCR5+/+ patients on HAART (Figure 1c) [ 16 ]. It is clear that latent HIV continues its pathogenesis in these patients, even in the presence of effective anti-retroviral treatment. We therefore need to develop better AIDS therapies.
Where does CCR5-32 occur?
The CCR5-Δ32 allele occurs at a relatively high frequency in Europe (about 10%), but is completely absent in native African and Asian people. This distribution, plus the high incidence of amino acid-altering mutations (about 80%) among all SNP variants in the CCR5 locus, lent support to the idea that CCR5-Δ32 was likely the object of strong selective pressures favoring CCR5-Δ32 frequency elevation in European ancestors [ 18, 71, 72 ]. The extended haplotype of SNPs around CCR5-Δ32 is about 1,000 kb, 100 times longer than the average haplotype size in Europeans, suggesting a recent mutational origin of CCR5-Δ32 and possibly a selective advantage of CCR5-Δ32 carriers [ 72 – 74 ].
What is cell and gene therapy?
Cell and Gene Therapy for HIV Cure. As the HIV pandemic rapidly spread worldwide in the 1980s and 1990s, a new approach to treat cancer, genetic diseases, and infectious diseases was also emerging. Cell and gene therapy strategies are connected with human pathologies at a fundamental level, by delivering DNA and RNA molecules that cou ….
When did HIV spread?
As the HIV pandemic rapidly spread worldwide in the 1980s and 1990s, a new approach to treat cancer, genetic diseases, and infectious diseases was also emerging. Cell and gene therapy strategies are connected with human pathologies at a fundamental level, by delivering DNA and RNA molecules that could correct and/or ameliorate ...