MediShare Review: A Christian Health Insurance Alternative

An encyclopedia of philosophy articles written by professional philosophers.

Dr. Danny B Corales, MD
He called in the new prescription on September 3. That part of our lives is over. HIV is different in structure from other retroviruses. I am looking at Medishare also and have the same questions as the person inquiring about whether payments to us are taxible? The Israel Medical Association journal: Core subjects are similar to biochemistry courses and typically include gene expression , research methods, proteins , cancer research, immunology , biotechnology and many more.

The path to neo-humanity as the foundation of the ideology of the “Evolution 2045” party

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Reconstructive challenges in the extended endoscopic transclival approach. Different clinical factors associated with Staphylococcus aureus and Pseudomonas aeruginosa in chronic rhinosinusitis.

Pediatric nasoseptal flap reconstruction for suprasellar approaches. Staphylococcus aureus triggers nitric oxide production in human upper airway epithelium. A Shield against Allergens? Two- versus four-handed techniques for endonasal resection of orbital apex tumors. Am J Rhinol Allergy. Sinus irrigations before and after surgery-Visualization through computational fluid dynamics simulations. Curr Allergy Asthma Rep. TAS2R38 genotype predicts surgical outcome in nonpolypoid chronic rhinosinusitis.

Contemporary management of esthesioneuroblastoma. Nodal metastasis and elective nodal level treatment in sinonasal small-cell and sinonasal undifferentiated carcinoma: Otolaryngol Head Neck Surg.

Cadaveric validation study of computational fluid dynamics model of sinus irrigations before and after sinus surgery. Propensity score analysis of endoscopic and open approaches to malignant paranasal and anterior skull base tumor outcomes. Analysis of surveillance methods in sinonasal malignancy.

A consistent landmark for superior septectomy during Draf III drill out. Correlation of T2R38 taste phenotype and in vitro biofilm formation from nonpolypoid chronic rhinosinusitis patients. Instrumentation in Frontal Sinus Surgery. Otolaryngol Clin North Am. Smell preservation following endoscopic unilateral resection of esthesioneuroblastoma: In vitro effects of anthocyanidins on sinonasal epithelial nitric oxide production and bacterial physiology.

Cerebrospinal fluid rhinorrhea secondary to idiopathic intracranial hypertension: Long-term outcomes of endoscopic repairs. Human upper airway epithelium produces nitric oxide in response to Staphylococcus epidermidis.

Expression of dermcidin in human sinonasal secretions. Risk of lymph node metastasis and recommendations for elective nodal treatment in squamous cell carcinoma of the nasal cavity and maxillary sinus: ILA and ILF are critical for antimicrobial peptide production and clearance of Staphylococcus aureus nasal colonization. Surgical and radiological anatomy of the paranasal sinuses. Recurrence and surveillance for sinonasal cancers.

Optimizing Outcomes and Avoiding Failures. Developmental Disorders of the Nose and Paranasal Sinuses. From the Lab to the Operating Room. Partial and Complete Ethmoidectomy.

Applied Physiology of the Paranasal Sinuses. Thieme Medical Publishers Inc. Biofilms in Chronic Rhinosinusitis. Diseases of the Sinuses: A Comprehensive Textbook of Diagnosis and Treatment.

Chang, Incaudo, Gershwin Editors. Disorders of the Orbit. Masters Technique in Otolaryngology- Rhinology. Traumatic Cerebrospinal Fluid Fistulas. Schwartz J, Adappa ND. A population may be important to epidemiologists but not to clinicians who must treat individual patients whose manifestation of a disease and response to therapy for that disease may differ from each other significantly.

The final notion of disease addresses this criticism. The genetic notion claims that disease is the mutation in or absence of a gene. Critics of the genetic notion claim that disease, especially its experience, cannot be reduced to nucleotide sequences. Instead, it requires a larger notion including social and cultural factors. The most common notion of health is simply absence of disease.

Health, according to proponents of this notion, represents a default state as opposed to pathology. In other words, if an organism is not sick then it must be healthy. Unfortunately, this notion does not distinguish between various grades of health or preconditions towards illness.

For example, as cells responsible for serotonin stop producing the neurotransmitter a person is prone to depression. Such a person is not as healthful as a person who is making sufficient amounts of serotonin. An adequate understanding of health should account for such preconditions. Moreover, health as absence of disease often depends upon personal and social values of what is health. Again, ambiguity enters into defining health given these values. For one person, health might be very different from that of another.

The second notion of health does permit distinction between grades of health, in terms of quantifying it, and does not depend upon personal or social values. Proponents of this notion, such as Boorse, define health in terms of normal functioning, where the normal reflects a statistical norm with respect to species design. For example, a person with low levels of serotonin who is not clinically symptomatic in terms of depression is not as healthful as a person with statistically normal neurotransmitter levels.

Criticisms of the second notion revolve around its lack of incorporating the social dimension of health and jettison the notion altogether opting for the notion of wellbeing. Epistemology is the branch of philosophy concerned with the analysis of knowledge, in terms of both its origins and justification.

The first pertains to knowledge by acquaintance, in which a knowing or an epistemic agent is familiar with an object or event. It is descriptive in nature, that is, a knowing-about knowledge. The second is competence knowledge, which is the species of knowledge useful for performing a task skillfully. It is performative or procedural in nature, that is, a knowing-how knowledge. Again, by way of example, the surgeon must know how to perform a specific surgical procedure before executing it.

The third, which interests philosophers most, is propositional knowledge. It pertains to certain truths or facts. This section begins with the debate between rationalists and empiricists over the origins of knowledge, before turning to medical thinking and explanation and then concluding with the nature of diagnostic and therapeutic knowledge.

The rationalism-empiricism debate has a long history, beginning with the ancient Greeks, and focuses on the origins of knowledge and its justification. As such, knowledge is intuitive in nature, and in contrast to the senses or perception, it is exclusively the product of the mind.

In other words, rationalism provides a firm foundation not only for the origin of knowledge but also for warranting its truth. Empiricists, such as Aristotle, Avicenna, Bacon, Locke, Hume, and Mill, avoid the fears of rationalists and exalt observation and experience with respect to the origin and justification of knowledge. Here, empiricists champion the role of experimentation in the origin and justification of knowledge.

The rationalism-empiricism debate originates specifically with ancient Greek and Roman medicine. Dogmatics relied on theory, especially the humoral theory of health and disease, to practice medicine.

The Empiric school of medicine, on the other hand, asserted that only observation and experience, not theory, is a sufficient foundation for medical knowledge and practice. Theory is an outcome of medical observation and experience, not their foundation. Empirics relied on palpable, not underlying, causes to explain health and disease and to practice medicine. Philinus of Cos and his successor Serapion of Alexandria, both third century BCE Greek physicians, are credited with founding the Empiric school, which included the influential Alexandrian school.

A third school of medicine arose in response to the debate between the Dogmatics and Empirics, the Methodic school of medicine. In contrast to Dogmatics, and in agreement with Empirics, Methodics argued that underlying causes are superfluous to the practice of medicine. The Dogmatism-Empiricism debate, with Methodism representing a minority position, raged on and was still lively in the seventeenth and eighteenth centuries.

For example, Giorgio Baglivi , an Armenian-born seventeenth century Italian physician, decried the polarization of physicians along dogmatic and empiric boundaries and recommended resolving the debate by combining the two.

Contemporary philosophical commentators on medicine recognize the importance of both epistemic positions, and several commentators propose synthesis of them. Although no clear resolution of the rationalism-empiricism debate in medicine appears on the immediate horizon, the debate does emphasize the importance of and the need for additional philosophical analysis of epistemic issues surrounding medical knowledge.

The first is by a medical humanities scholar, Kathryn Montgomery Montgomery addresses vital questions about how physicians go about making clinical decisions when often faced with tangible uncertainty. She argues for medical thinking based not on science but on Aristotelian phronesis, or practical or intuitive reasoning. The second book is by a practicing clinician, Jerome Groopman Groopman also addresses questions about medical thinking, and he too pleads for clinical reasoning based on practical or intuitive foundations.

Both books call for introducing the art of medical thinking to offset the over dependence on the science of medical thinking. In general, medical thinking reflects the cognitive faculties of clinicians to make rational decisions about what ails patients and how best to go about treating them both safely and effectively.

That thinking, during the twentieth century, mimicked the technical thinking of natural scientists—and, for good reason. As Paul Meehl convincingly demonstrated, statistical reasoning in the clinical setting out performs intuitive clinical thinking.

That analysis centers traditionally on both logical and algorithmic methods of clinical judgment and decision-making, to which the twenty-first century has turned.

However, not until the nineteenth century did logic of medicine become an important area of sustained analysis or have an impact on medical knowledge and practice. Contemporary logic of medicine continues this tradition, especially in terms of statistical analysis of experimental and clinical data. A particularly vigorous debate concerns the role of frequentist vs. Bayesian statistics in determining the statistical significance of data from clinical trials.

The logic of medicine, then, represents an important and a fruitful discipline in which medical scientists and clinical practitioners can detect and avoid errors in the generation and substantiation of medical knowledge and in its application or translation to the clinic. Philosophers of medicine actively debate the best courses of action for making clinical decisions.

To make such a judgment requires an insight into the intelligibility of the clinical evidence. The issue for philosophers of medicine is what role intuition should play in clinical judgment when facing the ideals of objective scientific reasoning and judgment. The debate often reduces to whether clinical judgment is an art or a science; however, some, like Alvan Feinstein , argue for a reconciliatory position between them.

Once a physician comes to a judgment then the physician must make a decision as to how to proceed clinically. Although clinical decision making, with its algorithmic-like decision trees, is a formal procedure compared to clinical judgment, philosophers of medicine actively argue about the structure of these trees and procedures for generating and manipulating them. The main issue is how best to define the utility grounding the trees.

Epistemologists are generally interested in the nature of propositions especially the explanatory power of those justified true beliefs. To know something truly is to understand and explain the hidden causes behind it. Explanations operate at a variety of levels. For example, neuroscientific explanations account for human behavior in terms of the neurological activity while astrological explanations account for such behavior with respect to astronomical activity.

Philosophers, especially philosophers of science, distinguish several kinds of explanations, including the covering law explanation, causal explanation, and inference to the best explanation.

This line of reasoning runs deep in medical history, beginning, as we have seen, with the Dogmatics. Twenty-first century philosophers of medicine utilize the explanatory schemes developed by philosophers of science to account for medical phenomena. The Following section will briefly examine each of these explanatory schemes and their relevance for medical explanations.

Carl Hempel and Paul Oppenheim introduced covering law explanation in the late s. According to Hempel and Oppenheim , explanations function as arguments with the conclusion or explanandum—that which is explained—deduced or induced from premises or explanans—that which does the explaining. At least one of the explanans must be a scientific law, which can be a mechanistic or statistical law.

Although covering law explanations are useful for those medical phenomena that reduce to mechanistic or statistical laws, such as explaining cardiac output in terms of heart rate and stroke volume, not all such phenomena lend themselves to such reductive explanations. The next explanatory scheme, causal explanation, attempts to rectify that problem. Causal explanation relies on the temporal or spatial regularity of phenomena and events and utilizes antecedent causes to explain phenomena and events.

The explanations can be simplistic in nature, with only a few antecedent causes arranged linearly, or very complex, with multiple antecedent causes operating in a matrix of interrelated and integrated interactions. For example, causal explanations of cancer involve at least six distinct sets of genetic factors controlling cellular phenomena such as cell growth and death, immunological response, and angiogenesis.

Finally, Gilbert Harman articulated the contemporary form of inference to the best explanation, or IBE, in the s. Harman proposed that based on the totality of evidence one must choose the explanation that best accounts for or infers that evidence and reject its competitors.

Donald Gillies provides an analysis of it in terms of Kuhnian paradigm. Diagnostic knowledge pertains to the clinical judgments and decisions made about what ails a patient. Epistemologically, the issues concerned with such knowledge are its accuracy and certainty. Central to both these concerns are clinical symptoms and signs. Clinical symptoms are subjective manifestations of the disease that the patient articulates during the medical interview, while clinical signs are objective manifestations that the physician discovers during the physical examine.

What is important for the clinician is how best to quantify those signs and symptoms, and then to classify them in a robust nosology or disease taxonomy. The clinician then narrows this set to one diagnostic hypothesis that best explains most, and hopefully all, of the relevant clinical evidence.

The epistemic mechanism that accounts for this process and the factors involved in it are unclear. Philosophers of medicine especially dispute the role of tacit factors in the process. Finally, the heuristics of the process are an active area of philosophical investigation in terms of identifying rules for interpreting clinical evidence and observations.

Therapeutic knowledge refers to the procedures and modalities used to treat patients. Epistemologically, the issues concerned with such knowledge are its efficacy and safety. Efficacy refers to how well the pharmacological drug or surgical procedure treats or cures the disease, while safety refers to possible patient harm caused by side effects. Although basic medical research into the etiology of disease mechanisms is important, the translation of that research and the philosophical problems that arise from it are foremost on the agenda for philosophers of medicine.

The origin of clinical trials dates at least to the eighteenth century but not until the twentieth century is consensus reached over the structure of these trials. Today, four phases define a clinical trial. During the first phase, clinical investigators establish the maximum tolerance of healthy volunteers to a drug. The following are topics of active discussion among philosophers of medicine: However, the most pressing problem is the type of statistics utilized for analyzing clinical trial evidence.

Some philosophers of medicine champion frequentist statistics, while others Bayesian statistics. Ethics is the branch of philosophy concerned with the right or moral conduct or behavior of a community and its members. Traditionally, philosophers divide ethics into descriptive, normative, and applied ethics. Descriptive ethics involves detailing ethical conduct without evaluating it in terms of moral codes of conduct, whereas normative ethics pertains to how a community and its members should act under given situations, generally in terms of an ethical code.

This code is often a product of certain values held in common within a community. For example, ethical codes against murder reflect values community members place upon taking human life without just cause. Besides values, ethicists base normative ethics on a particular theoretical perspective. Within western culture, three such perspectives predominate. The first and historically oldest ethical theory—although it experienced a Renaissance in the late twentieth century—is virtue ethics.

Virtue ethics claims that ethical conduct is the product of a moral agent who possesses certain virtues, such as prudence, courage, temperance, or justice—the traditional cardinal virtues.

The second ethical theory is deontology and bases moral conduct on adherence to ethical precepts and rules reflecting moral duties and obligations. The third ethical theory is consequentialism, which founds moral conduct on the outcome or consequence of an action. Finally, applied ethics is the practical use of ethics within a profession such as business or medicine.

Medical or biomedical ethics reflects applied ethics and is a major feature within the landscape of twenty-first century medicine. Historically, ethical issues are a conspicuous component of medicine beginning with Hippocrates. Throughout medical history several important treatises on medical ethics have been published. Today, medical ethics is founded not on any particular ethical theory but on four ethical principles. The origins of the predominant system for contemporary medical or biomedical ethics began in In that year, the Public Health Service, in conjunction with the Tuskegee Institute in Macon County, Alabama, undertook a clinical study to document the course of syphilis on untreated test subjects.

The subjects were Afro-American males. Over the next forty years, healthcare professionals observed the course of the disease, even after the introduction of antibiotics. What made the study so atrocious was that the healthcare professionals misinformed the subjects about treatment or failed to treat the subjects with antibiotics.

To insure that such flagrant abuse of test subjects did not happen again, the National Commission for the Protection of Human Subjects of Biomedical and Behavioral Research met from February , The outcome was a report entitled, Ethical Principles and Guidelines for the Protection of Human Subjects of Research , or known simply as the Belmont Report, published in The report lists and discusses several ethical principles necessary for protecting human test subjects and patients from unethical treatment at the hands of healthcare researchers and providers.

The next principle is beneficence or maximizing the benefits to risk ratio for the test subject. The final ethical principle is justice, which ensures that the cost to benefit ratio is equitably distributed among the general population and that no one segment of it bears an unreasonable burden with respect to the ratio. One of the framers of the Belmont Report was a young philosopher named Tom Beauchamp.

While working on the report, Beauchamp, in collaboration with a colleague, James Childress, was also writing a book on the role of ethical principles in guiding medical practice. Rather than ground biomedical ethics on any particular ethical theory, such as deontology or utilitarianism, Beauchamp and Childress looked to ethical principles for guiding and evaluating moral decisions and judgments in healthcare.

The fruit of their collaboration was Principles of Biomedical Ethics , first published in the same year as the Belmont Report, In the book, Beauchamp and Childress apply the ethical principles approach of the report to regulate the activities of biomedical researchers, to assist physicians in deliberating over the ethical issues associated with the practice of clinical medicine.

However, besides the three guiding principles of the report, they added a fourth—nonmaleficence. Moreover, the first principle became patient autonomy, rather than respect of persons as denoted in the report. Beauchamp and Childress articulate the final principle, justice, in terms reminiscent of the Belmont report with respect to equitable distribution of risks and benefits, as well as healthcare resources, among both the general and patient populations.

However, principlism is not without its critics. A fundamental complaint is the lack of theoretical support for the four principles, especially when the principles collide with one another in terms of their application to a bioethical problem. In its use, ethicists and clinicians generally apply the principles in an algorithmic manner to justify practically any ethical position on a biomedical problem.

What critics want is a unified theoretical basis for grounding the principles, in order to avoid or adjudicate conflicts among the principles. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Upon entry into the target cell, the viral RNA genome is converted reverse transcribed into double-stranded DNA by a virally encoded enzyme, reverse transcriptase , that is transported along with the viral genome in the virus particle.

The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded enzyme, integrase , and host co-factors. Alternatively, the integrated viral DNA may be transcribed , producing new RNA genomes and viral proteins, using host cell resources, that are packaged and released from the cell as new virus particles that will begin the replication cycle anew.

Two types of HIV have been characterized: HIV is different in structure from other retroviruses. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle. This is, in turn, surrounded by the viral envelope , that is composed of the lipid bilayer taken from the membrane of a human host cell when the newly formed virus particle buds from the cell. The viral envelope contains proteins from the host cell and relatively few copies of the HIV Envelope protein, [21] which consists of a cap made of three molecules known as glycoprotein gp , and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.

As the sole viral protein on the surface of the virus, the Envelope protein is a major target for HIV vaccine efforts. The density is high as the glycans shield the underlying viral protein from neutralisation by antibodies.

This is one of the most densely glycosylated molecules known and the density is sufficiently high to prevent the normal maturation process of glycans during biogenesis in the endoplasmic and Golgi apparatus. The molecular structure of the viral spike has now been determined by X-ray crystallography [29] and cryogenic electron microscopy. Three of these genes, gag , pol , and env , contain information needed to make the structural proteins for new virus particles.

The six remaining genes, tat , rev , nef , vif , vpr , and vpu or vpx in the case of HIV-2 , are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus replicate , or cause disease. Nef also interacts with SH3 domains. The vpu protein p16 influences the release of new virus particles from infected cells. Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell.

The Psi element is involved in viral genome packaging and recognized by gag and rev proteins. The term viral tropism refers to the cell types a virus infects. Indeed, macrophages play a key role in several critical aspects of HIV infection. Macrophages and microglial cells are the cells infected by HIV in the central nervous system.

In the tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus. Some people are resistant to certain strains of HIV. Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid , which enables the virus to be transmitted from a male to his sexual partner.

The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process [ further explanation needed ] leads to a predominant transmission of the R5 virus through this pathway.

A number of studies with subtype B-infected individuals have determined that between 40 and 50 percent of AIDS patients can harbour viruses of the SI and, it is presumed, the X4 phenotypes. The adoption of "accessory genes" by HIV-2 and its more promiscuous pattern of co-receptor usage including CD4-independence may assist the virus in its adaptation to avoid innate restriction factors present in host cells. Adaptation to use normal cellular machinery to enable transmission and productive infection has also aided the establishment of HIV-2 replication in humans.

A survival strategy for any infectious agent is not to kill its host, but ultimately become a commensal organism. Having achieved a low pathogenicity, over time, variants that are more successful at transmission will be selected. Entry to the cell begins through interaction of the trimeric envelope complex gp spike on the HIV viral envelope and both CD4 and a chemokine co-receptor generally either CCR5 or CXCR4 , but others are known to interact on the target cell surface.

The first step in fusion involves the high-affinity attachment of the CD4 binding domains of gp to CD4. Once gp is bound with the CD4 protein, the envelope complex undergoes a structural change, exposing the chemokine receptor binding domains of gp and allowing them to interact with the target chemokine receptor. This loop structure brings the virus and cell membranes close together, allowing fusion of the membranes and subsequent entry of the viral capsid.

After HIV has bound to the target cell, the HIV RNA and various enzymes, including reverse transcriptase, integrase, ribonuclease, and protease, are injected into the cell. They are currently thought to play an important role by transmitting HIV to T cells when the virus is captured in the mucosa by DCs.

HIV-1 entry, as well as entry of many other retroviruses, has long been believed to occur exclusively at the plasma membrane. More recently, however, productive infection by pH -independent, clathrin-mediated endocytosis of HIV-1 has also been reported and was recently suggested to constitute the only route of productive entry. Shortly after the viral capsid enters the cell, an enzyme called reverse transcriptase liberates the positive-sense single-stranded RNA genome from the attached viral proteins and copies it into a complementary DNA cDNA molecule.

The integration of the viral DNA into the host cell's genome is carried out by another viral enzyme called integrase. These mRNAs are exported from the nucleus into the cytoplasm , where they are translated into the regulatory proteins Tat which encourages new virus production and Rev. As the newly produced Rev protein is produced it moves to the nucleus, where it binds to full-length, unspliced copies of virus RNAs and allows them to leave the nucleus. Gag proteins bind to copies of the virus RNA genome to package them into new virus particles.

Upon infection and replication catalyzed by reverse transcriptase, recombination between the two genomes can occur. This form of recombination is known as copy-choice. Recombination events may occur throughout the genome. Anywhere from two to 20 recombination events per genome may occur at each replication cycle, and these events can rapidly shuffle the genetic information that is transmitted from parental to progeny genomes.

Viral recombination produces genetic variation that likely contributes to the evolution of resistance to anti-retroviral therapy. Yet, for the adaptive advantages of genetic variation to be realized, the two viral genomes packaged in individual infecting virus particles need to have arisen from separate progenitor parental viruses of differing genetic constitution.

It is unknown how often such mixed packaging occurs under natural conditions. In addition, Hu and Temin [72] suggested that recombination is an adaptation for repair of damage in the RNA genomes.

Strand switching copy-choice recombination by reverse transcriptase could generate an undamaged copy of genomic DNA from two damaged single-stranded RNA genome copies. This view of the adaptive benefit of recombination in HIV could explain why each HIV particle contains two complete genomes, rather than one. Furthermore, the view that recombination is a repair process implies that the benefit of repair can occur at each replication cycle, and that this benefit can be realized whether or not the two genomes differ genetically.

On the view that recombination in HIV is a repair process, the generation of recombinational variation would be a consequence, but not the cause of, the evolution of template switching. HIV-1 infection causes chronic inflammation and production of reactive oxygen species. For HIV, as well as for viruses in general, successful infection depends on overcoming host defensive strategies that often include production of genome-damaging reactive oxygen species.

Thus, Michod et al. The final step of the viral cycle, assembly of new HIV-1 virions, begins at the plasma membrane of the host cell. The Env polyprotein gp goes through the endoplasmic reticulum and is transported to the Golgi apparatus where it is cleaved by furin resulting in the two HIV envelope glycoproteins, gp41 and gp The Gag p55 and Gag-Pol p polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell.

The budded virion is still immature as the gag polyproteins still need to be cleaved into the actual matrix, capsid and nucleocapsid proteins. This cleavage is mediated by the packaged viral protease and can be inhibited by antiretroviral drugs of the protease inhibitor class.

The various structural components then assemble to produce a mature HIV virion. The classical process of infection of a cell by a virion can be called "cell-free spread" to distinguish it from a more recently recognized process called "cell-to-cell spread". Firstly, an infected T cell can transmit virus directly to a target T cell via a virological synapse. HIV differs from many viruses in that it has very high genetic variability.

This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day. When simultaneous infection occurs, the genome of progeny virions may be composed of RNA strands from two different strains. This hybrid virion then infects a new cell where it undergoes replication. As this happens, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes.

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