Public health genomics is the use of genomics information to benefit public health. This is visualized as more effective preventive care and disease treatments with better specificity, tailored to the genetic makeup of each patient. According to the Centers for Disease Control and Prevention (U.S.), Public Health genomics is an emerging field of study that assesses the impact of genes and their interaction with behavior, diet and the environment on the population's health. This field of public health genomics is less than a decade old. A number of think tanks, universities, and governments (including the U.S., UK, and Australia) have started public health genomics projects. Research on the human genome is generating new knowledge that is changing public health programs and policies. Advances in genomic sciences are increasingly being used to improve health, prevent disease, educate and train the public health workforce, other healthcare providers, and citizens.
Public policy Public policy has protected people against genetic discrimination, defined in Taber's Cyclopedic Medical Dictionary (2001) as unequal treatment of persons with either known genetic abnormalities or the inherited propensity for disease; genetic discrimination may have a negative effect on employability, insurability and other socio-economic variables. Public policy in the U.S. that protect individuals and groups of people against genetic discrimination include the Americans with Disabilities Act of 1990, Executive Order 13145 (2000) that prohibits genetic discrimination in the workplace for federal employees, and the Genetic Information Nondiscrimination Act of 2008. Main public concerns regarding genomic information are that of confidentiality, misuse of information by health plans, employers, and medical practitioners, and the right of access to genetic information. Concerns also exist about the equitable deployment of public health genomics, and attention is needed to ensure that the implementation of genomic medicine does not further entrench social‐equity concerns.
Ethical concerns One of the many facets involved in public health genomics is that of bioethics. This has been highlighted in a study in 2005 by Cogent Research, that found when American citizens were asked what they thought the strongest drawback was in using genetic information, they listed "misuse of information/invasion of privacy" as the single most important problem. In 2003, the Nuffield Council on Bioethics published a report, Pharmacogenetics: Ethical Issues. Authors of the document explore four broad categories of ethical and policy issues related to pharmacogenetics: information, resource, equity and control. In the introduction to the report, the authors clearly state that the development and application of pharmacogenetics depend on scientific research, but that policy and administration must provide incentives and restraints to ensure the most productive and just use of this technology. Involving the public in ethical oversight and other ways can improve public trust in public health genomics as well as acceptability of initiatives and ensuring that access to the benefits of genomics research is equitable.
Genetic susceptibility to disease Single nucleotide polymorphisms (SNPs) are single bases within a gene sequence that differ from that gene's consensus sequence, and are present in a subset of the population. SNPs may have no effect on gene expression, or they can change the function of a gene completely. Resulting gene expression changes can, in some cases, result in disease, or in susceptibility to disease (e.g., viral or bacterial infection). Some current tests for genetic diseases include: cystic fibrosis, Tay–Sachs disease, amyotrophic lateral sclerosis (ALS), Huntington's disease, high cholesterol, some rare cancers and an inherited susceptibility to cancer. A select few are explored below.
Herpesvirus and bacterial infections Since the field of genomics takes into account the entire genome of an organism, and not simply its individual genes, the study of latent viral infection falls into this realm. For example, the DNA of a latent herpesvirus integrates into the host's chromosome and propagates through cell replication, although it is not part of the organism's genome, and was not present at the birth of the individual. An example of this is found in a study published in Nature, which showed that mice with a latent infection of a herpesvirus were less susceptible to bacterial infections. Murine mice were infected with murine gammaherpesvirus 68 and then challenged with the Listeria monocytogenes bacterium. Mice that had a latent infection of the virus had an increased resistance to the bacteria, but those with a non-latent strain of virus had no change in susceptibility to the bacteria. The study went on to test mice with murine cytomegalovirus, a member of the betaherpesvirinae subfamily, which provided similar results. However, infection with human herpes simplex virus type-1 (HSV-1), a member of the alphaherpesvirinae subfamily, did not provide increased resistance to bacterial infection. They also used Yersinia pestis (the causative agent of the Black Death) to challenge mice with a latent infection of gammaherpesvirus 68, and they found the mice did have an increased resistance to the bacteria. The suspected reason for this is that peritoneal macrophages in the mouse are activated after latent infection of the herpesvirus, and since macrophages play an important role in immunity, this provides the mouse with a stronger, active immune system at the time of bacterial exposure. It was found that the latent herpesvirus caused an increase in interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), cytokines which both lead to activation of macrophages and resistance to bacterial infection.
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