This presentation is introductory in nature and is intended only to bring attention to a new disease entity that has not been previously reported. Attention is drawn herein to general manifestations of the initial pathology in a number of cases. No discussion of medical history, treatments, or outcome will be attempted at this time since most cases have not been satisfactorily resolved. These aspects will be discussed at a later date on a case by case basis as further progress allows and as more detailed information becomes available.

The Bacteria Cyclogeny1 is the morphological developmental cycle through the sum of all generations, beginning with the simplest morphological unit (Mych, Mychit or Mychomerit) to the highest morphological structure pertinent to each particular species, ending again with the unit Mychit or Mychomerit. This is, a phylogenetically high form takes its course, starting from the Mychit to the Dimychit and all appearance forms of the Syndimychit, up to the syntact Syndimychit, and back to the Mych -- usually with the tiniest step forward being distributed over numerous generations.

Patients with chronic fatigue syndromes (primary fibrositis syndrome, major affective disorder, etc.) have elevated IgG serum antibodies to multiple common viruses. Only IgG rubella antibodies are positively correlated with the intensity of symptoms and have a height that is clearly significant compared to healthy controls. The lymphotropic properties of the rubella virus could account for the multiple elevated antibodies. Adult women are over﷓represented in the population of patients with chronic fatigue, and are especially susceptible to developing such symptoms following exposure to attenuated rubella virus. A new more potent strain of live rubella vaccine (strain RA27/3) was introduced in 1979. Within three years reports of patients with chronic fatigue began surfacing in the literature. Considering all this, the possible role of rubella immunization in the etiology of chronic fatigue syndromes deserves further study.

A monkey virus that scientists have long thought does not infect humans has been detected in human tumors, but whether the virus caused the tumors has not been proven. "Evidence is mounting that simian virus 40 (SV40) infects humans and is associated with certain types of human tumors," said Dr. Janet Butel, head of the division of molecular virology at Baylor College of Medicine in Houston. "This association with human disease might lead to new approaches for diagnosing and treating certain types of cancers and other illnesses, but further studies are needed to determine whether SV40 plays a causative role in the tumors," she said. Butel and Dr. John Lednicky, also a Baylor molecular virologist, presented an overview of what is known about SV40 in the Jan. 20 issue of the Journal of the National Cancer Institute.

Division of Molecular Virology, Baylor College of Medic

Polyomaviruses are small DNA viruses that typically establish persistent but inapparent infections of their natural hosts, although cytolytic disease may develop if the host becomes immunocompromised. Most polyomaviruses have the ability to induce tumor formation when introduced into certain foreign hosts and are considered oncoviruses. Some polyomaviruses, including those that infect humans, have occasionally been detected in cancerous tissue of their natural hosts. This article briefly reviews the biology of polyomaviruses (in particular-BK virus (BKV), JC virus (JCV), simian virus 40 (SV40.)The most intensely studied viruses in this group are PyV and SV40 (3and explores issues pertaining to the significance of association of polyomaviruses with human tumors.

Human herpesvirus-6 was discovered in 1986. Since then, a considerable amount of research information has been published regarding this fascinating virus. The role of this relatively new member of the herpes family in human disease continues to be defined. It is now widely accepted that primary infection results in roseola (erythema subitum). The virus can also cause a mononucleosis-like syndrome in older children and adults. HHV-6 has now been associated with a variety of potentially life-threatening infectious complications in the immune compromised host. Numerous serious neurologic conditions have been described in both the normal host (children and adults), and the immune compromised host. The virus is clearly neurotropic and immunotropic. Recent evidence also suggests tropism and infection of endothelial cells.

CHRONIC FATIGUE SYNDROME (CFS), like fibromyalgia and multiple chemical sensitivity,comprises a number of poorly under-stood signs and symptoms, and whether a patient receives the diagnosis for one or another of these symptom clusters may depend on the specialty of the physician making the diagnosis. Patients with CFS also often fulfill case definitions for these other illnesses. This overlap suggests that these “functional somatic illnesses” may be variants of one another. However, this does not necessarily mean that these syndromes share the same pathobiological processes or causes. For example, patients with fibromyalgia have been found to have elevated levels of substance P in spinal fluid 3 and reduced pain thresholds, while patients with CFS have not. Similarly, the fatigue reported by patients with fibromyalgia may be secondary to chronic sleep disruption because of pain, while fatigue may be primary in CFS. The case definitions for CFS reflect the observation that the severe fatigue and influenza-like symptoms, which often begin suddenly, were initially thought to represent an underlying viral infection. Thus, the diagnosis requires at least 6 months of new onset symptoms of fatigue accompanied by infectious, rheumatlogical, and neuropsychiatric symptoms,and which cannot be explained by other medical diagnoses. In the United States, CFS has a prevalence of 0.52% in women and 0.29% in men. Patients with CFS may experience severe disability; one study reported that patients with CFS have lower self-reported functional status than a group of similar patients with congestive heart failure. In this article, I review the evidence about the etiology of CFS.

There is now significant literature showing that Psychological Stress can down-regulate various aspects of the Cellular Immune Response. It is also established that communication between the Central Nervous System and the Immune System occurs through bidirectional signals linking the Nervous, Endocrine, and Immune Systems. Psychological Stressors affect the Immune System by disrupting these networks. In this overview, we discuss the implications of Psychological Stress-Associated Immune Modulation and risk for infectious disease.