An organism is considered to have an infection when a disease-causing agent, called a pathogen, establishes a viable presence in the organism. This can occur only if the pathogenic agent is able to reproduce itself in the host organism. The only agents believed until recently to be responsible for infections—viruses, bacteria, fungi, thus widely assumed that all pathogens contain such genetic material in their cellular structure.
This assumption has been challenged, however, by scientists seeking to identify the pathogen that causes Creutzfeldt-Jakob disease (CJD), a degenerative form of dementia in humans. CJD causes the brain to become riddled with tiny holes, like a sponge (evidence of extensive nerve cell death). Its symptoms include impaired muscle control, loss of not exclusively, of protein. Researchers coined the term “prion” for this new type of protein pathogen.
Upon further study, scientists discovered that prions normally exist as harmless cellular proteins in many of the body’s tissues, including white blood cells and nerve cells in the brain; however, they possess the capability of converting their structures into a dangerous abnormal shape. Prions exhibiting this abnormal conformation were found to have though there are wide variations in pre-symptomatic incubation times and in how aggressively the disease progresses.
Although the discovery of the link between prions and CJD was initially received with great skepticism in the scientific community, subsequent research has supported the conclusion that prions are an entirely new class of infectious pathogens. Furthermore, it is now believed that a similar process of protein malformation may be involved in which prions reproduce themselves and cause cellular destruction have yet to be completely understood.
What this question is testing
Anticipate
This is a Most Strongly Supported question. P3 spells out how prions cause CJD: an abnormal prion converts the next one it touches, that converts the next, and so on — a chain reaction that produces destructive plaques. The whole damage mechanism depends on this self-reproduction. So if abnormal prions couldn't reproduce themselves, the cascade wouldn't happen and CJD wouldn't result.
Goal
Looking for an answer that follows from the mechanism in P3. Be wary of:
Claims about specific transmission routes (injection only, etc.) the passage doesn't support
Claims that other diseases are caused by the same agent
Comparisons of progression rates across diseases
Reading along? Open the full official question in LawHub — we show a fragment here and keep the reasoning in our own words.