Filtrable Virus Research Articles

Landry's rabies and paralysis

In recent years, more and more generalizations have begun to be made between clinically different diseases caused by filterable and ultramicroscopic viruses. Such Schiikrin Spatz point to the similarity of the pathological and anatomical picture between rabies and acute epidemic encephalitis, which is so great that without knowledge of the anamnesis and clinical course, it is impossible to know which disease is in question.

VIRAL ETIOLOGY OF LEUKEMIA AND LYMPHOMAS.

CONSIDERABLE PROGRESS has been accomplished during the past 15 years in the study of the nature of leukemia. It seems more and more apparent that the various forms of leukemia and lymphomas, not only in chickens, mice, rats, and other animal species, but also in humans, are caused by filterable and transmissible viruses.

The History of Mycoplasma pneumoniae Pneumonia.

In the United States in the 1930s, although the pathogen was not known, atypical pneumonia was clinically distinguished from pneumococcal pneumonia by its resistance to sulfonamides. Reimann (1938) reported seven patients with an unusual form of tracheo bronchopneumonia and severe constitutional symptoms. He believed the clinical picture of this disease differed from that of the disease caused by influenza viruses or known bacteria and instead suspected “primary atypical pneumonia.” For many years, the responsible infectious agent was tentatively classified as a filterable virus that could pass through a Seitz filter to remove bacteria and was reported to be a psittacosis-like or new virus. After that, Eaton et al. (1942, 1944, 1945) identified an agent that was the principal cause of primary atypical pneumonia using cotton rats, hamsters, and chick embryos. Eaton et al. (1942, 1944, 1945) did not perform an inoculation study in human volunteers. During the 1940s, there were three groups engaged in discovering the etiology of the primary atypical pneumonia. (1) Commission on Acute Respiratory Diseases Diseases directed by John Dingle, (2) Dr. Monroe Eaton’s group, the Virus Research Laboratory of the California State Public Health Department, (3) The Hospital of the Rockefeller Institute for Medical Research directed by Horsfall. During 1940s, the members of the Commission on Acute Respiratory Diseases concluded that the bacteria-free filtrates obtained from the patients, presumably containing a virus, could induce primary atypical pneumonia in human volunteers via Pinehurst trials. During 1950s, serological approaches for identification of the Eaton agent developed such as Fluorescent-Stainable Antibody, and at the beginning of the1960s, the Eaton agent successfully grew in media, and finally accepted as a cause of primary atypical pneumonia. Thus, technical difficulties with visualizing the agent and failure to recognize the full significance of the Pinehurst transmission experiments resulted in a lapse of 20 years before acceptance of the Eaton agent as Mycoplasma pneumoniae. This review describes the history of M. pneumoniae pneumonia with a special focus on the recognition between the 1930 and 1960s of the Eaton agent as the infectious cause.

Inventing Viruses.

In the nineteenth century, "virus" commonly meant an agent (usually unknown) that caused disease in inoculation experiments. By the 1890s, however, some disease-causing agents were found to pass through filters that retained the common bacteria. Such an agent was called "filterable virus," the best known being the virus that caused tobacco mosaic disease. By the 1920s there were many examples of filterable viruses, but no clear understanding of their nature. However, by the 1930s, the term "filterable virus" was being abandoned in favor of simply "virus," meaning an agent other than bacteria. Visualization of viruses by the electron microscope in the late 1930s finally settled their particulate nature. This article describes the ever-changing concept of "virus" and how virologists talked about viruses. These changes reflected their invention and reinvention of the concept of a virus as it was revised in light of new knowledge, new scientific values and interests, and new hegemonic technologies.

When viruses were not in style: Parallels in the histories of chicken sarcoma viruses and bacteriophages

The discovery that cancer may be caused by viruses occurred in the early twentieth century, a time when the very concept of viruses as we understand it today was in a considerable state of flux. Although certain features were agreed upon, viruses, more commonly referred to as ‘filterable viruses’ were not considered much different from other microbes such as bacteria except for their extremely small size, which rendered them ultramicroscopic and filterable. For a long time, in fact, viruses were defined rather by what they were not and what they could not do, rather than any known properties that set them apart from other microbes. Consequently when Peyton Rous suggested in 1912 that the causative agent of a transmissible sarcoma tumor of chickens was a virus, the medical research community was reluctant to accept his assessment on the grounds that cancer was not infectious and was caused by a physiological change within the cells. This difference in the bacteriological and physiological styles of thinking appears to have been prevalent in the wider research community, for when in 1917 Felix d'Herelle suggested that a transmissible lysis in bacteria, which he called bacteriophagy, was caused by a virus, his ideas were also opposed on similar grounds. It was not until the 1950s when when André Lwoff explained the phenomenon of lysogeny through his prophage hypothesis that the viral identities of the sarcoma-inducing agent and the bacteriophages were accepted. This paper examines the trajectories of the curiously parallel histories of the cancer viruses and highlights the similarities and differences between the ways in which prevailing ideas about the nature of viruses, heredity and infection drove researchers from disparate disciplines and geographic locations to develop their ideas and achieve some consensus about the nature of cancer viruses and bacteriophages.

Chapter 1 - A history of viral infections of the central nervous system: foundations, milestones, and patterns

For millennia, infectious diseases were viewed as the result of malignant supernatural forces or punishments by angry gods for human transgressions. In the 19th century several advances occurred. Medicine became based on clinical observations; Rudolph Virchow laid the foundation of cellular pathology; Louis Pasteur dismantled the notion of spontaneous generation, and Robert Koch established the fundamental techniques of bacteriology, together creating the revolutionary paradigm shift of germ theory. Virology was born in the last decade of the 19th century in the study of tobacco mosaic virus; the crucial characteristics were the capacity to pass through a bacteria-retaining filter and the need for living cells in which to replicate. In 1901 yellow fever was shown to be the first human disease to be caused by a “filterable virus.” In 1903 rabies would be the first disease of the nervous system to be determined to be viral in nature, and polio followed soon thereafter. Paradoxically, because no agent has yet been shown to be the cause, the modern study of epidemic encephalitis began with encephalitis lethargica in 1917. However, the flood gates of viral isolations opened in the 1930s for the arboviral encephalitides, using experimental primates and mice, starting with St. Louis encephalitis and Japanese encephalitis. Within a decade, the viral nature of aseptic meningitis and herpes simplex sporadic encephalitis was demonstrated. From the 1950s through the 1970s great interest in “slow viral diseases” arose as potential models for chronic diseases of the nervous system. The era of modern neurovirology has been characterized by two principal features. The first is the remarkable advances in technology – witness the use of polymerase chain reaction (PCR) for identifying infectious agents, magnetic resonance imaging (MRI) to image the nervous system, and the advance in therapeutics based on molecular medicine. The second has been the impact of emerging and re-emerging diseases – witness the human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) epidemic, Nipah encephalitis, and the appearance of West Nile encephalitis in the western hemisphere.

Lifelong Curiosity: Frederick Novy and the Rat Virus

Frederick Novy (1864-1957) was a U.S. physician, medical researcher, and influential microbiologist of the early 20th century who devised culture techniques to visualize anaerobic bacteria, parasites, and spirochetes. In 1909 he began to investigate the cause of unexplained deaths in his laboratory rats, which he hypothesized were due to an "ultramicroscopic organism" or "filterable virus." But in 1918, the test tubes he had been using for these experiments vanished from his laboratory. His dream of finding a virus as the likely cause of the mysterious deaths of his rats apparently was lost. Novy retired in 1935. Thirty-three years later, in 1951, a box containing the test tubes was discovered by chance during clean-up in preparation for a laboratory move. Novy's curiosity had not waned with time. Notified of the find, and 16 years into his retirement, he returned to his laboratory at the age of 88 to continue the experiments that he had begun more than 40 years earlier. He completed his investigations in 1953 and published his findings that a virus was indeed the unidentified organism that had swiftly killed his laboratory rats in 1909.

The history of avian influenza

The first description of avian influenza (AI) dates back to 1878 in northern Italy, when Perroncito [Perroncito E. Epizoozia tifoide nei gallinacei. Annali Accad Agri Torino 1878;21:87-126] described a contagious disease of poultry associated with high mortality. The disease, termed "fowl plague", was initially confused with the acute septicemic form of fowl cholera. However, in 1880, soon after its first description, Rivolta and Delprato [as reported by Stubs EL. Fowl pest, In: Biester HE, Devries L, editors. Diseases of poultry. 1st ed. Ames, IO: Iowa State College Press; 1943. p. 493-502] showed it to be different from fowl cholera, based on clinical and pathological properties, and called it Typhus exudatious gallinarum. In 1901, Centanni and Savunzzi [Centanni E, Savonuzzi E, La peste aviaria I & II, Communicazione fatta all'accademia delle scienze mediche e naturali de Ferrara, 1901] determined that fowl plague was caused by a filterable virus; however, it was not until 1955 that the classical fowl plague virus was shown to be a type A influenza virus based on the presence of type A influenza virus type-specific ribonucleoprotein [Schäfer W. Vergleichender sero-immunologische Untersuchungen über die Viren der Influenza und klassischen Geflügelpest. Z Naturf 1955;10b:81-91]. The term fowl plague was substituted by the more appropriate term highly pathogenic avian influenza (HPAI) at the First International Symposium on Avian Influenza [Proceedings of the First International Symposium on Avian Influenza. Beltsville, MD. 1981, Avian Dis 47 (Special Issue) 2003.] and will be used throughout this review when referring to any previously described fowl plague virus.

<char aid="99871517" id="ital">Furor Therapeuticus</char>: Benjamin Rush and the Philadelphia Yellow Fever Epidemic of 1793

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A medicina e a influenza espanhola de 1918

No início do século XX, a pandemia de gripe espanhola suscitou uma ampla discussão em meio à comunidade cientifica internacional a respeito da sua natureza e do seu agente causal. Através deste artigo, buscamos apresentar algumas das controvérsias que marcaram os debates médicos em torno desta manifestação da influenza, abordando as teorias pré-bacterianas e a noção bacteriana da doença, destacando a proposição de Pfeiffer e a suposição da ação de agentes invisíveis, então chamados vírus filtráveis.

Fish bile and cautery: trachoma treatment in art

Fish bile and cautery: trachoma treatment in art

The Early History of Infectious Bronchitis

Two years later, Bushnell and Brandly (3) reported on an essentially identical disease. They established that the causative agent was a filterable virus because the disease could be transmitted by Berkefeld-filtered material. Because the symptoms of respiratory distress were caused by a filterable virus, Bushnell and Brandly regarded the disease as a form of infectious laryngotracheitis (LT). Further critical tests were not made to confirm this identity. Bushnell and Brandly's report (3) was considered by most later research workers in avian respiratory diseases to actually describe further outbreaks of infectious bronchitis (IB). It was not until much later that the possibility could be considered that some or all of their cases could really have been cases of the mild or lowvirulence type of LT described by Cover and Benton (4). A further source of confusion was that, in the 1930s, the name infectious bronchitis was used in some papers actually describing LT. This confusion was cleared up a few years later by Beach and Schalm (1), who proved by cross-immunity studies in chickens that IB virus was distinct from infectious LT virus and

Increased CSF and brain quinolinic acid in schizophrenia and bipolar disorder

For millennia, infectious diseases were viewed as the result of malignant supernatural forces or punishments by angry gods for human transgressions. In the 19th century several advances occurred. Medicine became based on clinical observations; Rudolph Virchow laid the foundation of cellular pathology; Louis Pasteur dismantled the notion of spontaneous generation, and Robert Koch established the fundamental techniques of bacteriology, together creating the revolutionary paradigm shift of germ theory.Virology was born in the last decade of the 19th century in the study of tobacco mosaic virus; the crucial characteristics were the capacity to pass through a bacteria-retaining filter and the need for living cells in which to replicate. In 1901 yellow fever was shown to be the first human disease to be caused by a “filterable virus.” In 1903 rabies would be the first disease of the nervous system to be determined to be viral in nature, and polio followed soon thereafter.Paradoxically, because no agent has yet been shown to be the cause, the modern study of epidemic encephalitis began with encephalitis lethargica in 1917. However, the flood gates of viral isolations opened in the 1930s for the arboviral encephalitides, using experimental primates and mice, starting with St. Louis encephalitis and Japanese encephalitis. Within a decade, the viral nature of aseptic meningitis and herpes simplex sporadic encephalitis was demonstrated. From the 1950s through the 1970s great interest in “slow viral diseases” arose as potential models for chronic diseases of the nervous system.The era of modern neurovirology has been characterized by two principal features. The first is the remarkable advances in technology – witness the use of polymerase chain reaction (PCR) for identifying infectious agents, magnetic resonance imaging (MRI) to image the nervous system, and the advance in therapeutics based on molecular medicine. The second has been the impact of emerging and re-emerging diseases – witness the human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) epidemic, Nipah encephalitis, and the appearance of West Nile encephalitis in the western hemisphere.

Dissolving microbes in dissension

Antony Twort, In Focus, Out of Step: A Biography of Frederick William Twort F.R.S . Alan Sutton Publishing Ltd. Stroud, 1993. pp. xii + 340. £25. ISBN 0-7509-0327-9. Most microbiologists, remarks the author in this biography of his father, have heard of the Twort-d' Hérelle phenomenon , filterable viruses that lyse bacteria (bacteriophages). In 1915, F.W. (Peter) Twort published a paper in the Lancet in which he described the way in which ‘dissolving material’ obtained from bacterial cultures produced transparent patches in bacterial colonies. He also remarked that such clear patches (now described as plaques) sometimes appeared spontaneously in plate cultures. Jacques Senez, in his microbiology textbook of 1968, commented that this paper described all the essential characteristics of bacteriophages.

A Review of Techniques for the Serologic Diagnosis of Equine Infectious Anemia

History and introduction This paper will review the current serologic tests to Equine infectious anemia (EIA) has been recognized diagnose infections with EIAV, discuss limitations of as an important viral disease of members of the horse the procedures, and suggest improvements based on family since its “filterable virus” etiology was proven early in the twentieth century. Only since the 1970s EIAV and the horse have we been able to diagnose infection with equine infectious anemia virus (EIAV) accurately with the use The EIAV is a member of the lentivirus subfamily of serodiagnostic methods. Early attempts to define of retroviruses and shares morphologic, antigenic, and specific diagnostic tools for EIA failed in part because genetic characters with the other lentiviruses. 17 The of a lack of suitable in vivo laboratory animal models major core protein of EIAV is a product of the viral and in vitro techniques for virus propagation, as well gag gene, 45 has a molecular weight of 26,000 daltons as the tendency of EIAV to undergo “antigenic drift.” (p26), 37 represents about 40% of the virion mass, The recognition of the highly mutable typeor subtypeand has group and interspecies antigenic determispecific antigens of EIAV which stimulated neutraliznants. 12,30,31 The major core protein appears to be highing antibodies suggested that a widely applicable diagly conserved between EIAV isolates, 44 and the imnostic test for the disease would not be forthcoming. munodominant regions of the protein have been Complement fixation and precipitin tests were tried elucidated. 4 Antibodies to the major core protein are but held little promise as accurate and/or practical didetected in the AGID test because the p26 antigen agnostics. 21,43 Horse inoculation tests were standardpredominates in antigen preparations. Occasional reized for the diagnosis of EIA, but were expensive, actions to the pl5 protein of EIAV have been noted wasteful of equine resources and required facilities in in the AGID test. 25,47

Landmark article Dec 24,1938: An acute infection of the respiratory tract with atypical pneumonia. A disease entity probably caused by a filtrable virus. By Hobart A. Reimann

Landmark article Dec 24,1938: An acute infection of the respiratory tract with atypical pneumonia. A disease entity probably caused by a filtrable virus. By Hobart A. Reimann

An Acute Infection of the Respiratory Tract With Atypical Pneumonia

Infections of the respiratory tract are among the most common afflictions of mankind, and pneumonia, which occasionally accompanies or follows them, is the third most common cause of death in the United States. Any progress made in the knowledge of such infections is therefore urgently needed. Only recently has the physician been armed with comparatively simple methods for the diagnosis of one of these diseases, epidemic influenza, which is now known to be caused by a filtrable virus. Methods for isolating and identifying the virus of the common cold are still too complicated for the average clinical laboratory in routine diagnosis. The discovery of the causative agent of influenza permits separation of the disease as an entity from the undifferentiated group of infections of the respiratory tract and provides a standard, so to speak, against which other entities may be compared. The discovery also confirmed a long established impression gained

ISOLATION OF VIRUS FROM THE SPINAL FLUID OF THREE PATIENTS WITH MULTIPLE SCLEROSIS AND ONE WITH AMYOTROPHIC LATERAL SCLEROSIS

A transmissible agent with the properties of a thermolabile filterable virus was isolated from the cerebrospinal fluid (CSF) of 4 Houston patients with chronic central nervous system (CNS) disease. 3 had multiple sclerosis and 1 had amyotrophic lateral sclerosis. No isolations were made from 27 patients whose CSF was taken for diagnosis of illness unrelated to degenerative CNS disease. Neutralising antibodies to the 4 isolates were present in the serum of each of the 4 patients with virus (14 positive results among 15 tests) but in hardly any of the sera from 8 patients without virus (3 antibody-positive results among 32 tests). The agent is antigenically related to the virus isolated in Japan from cases of subacute myelo-optico-neuropathy.

The Role of C-Type and Other Oncogenic Virus Particles in Cancer and Leukemia

During the first half of this century, cancer and allied diseases were generally thought to be caused by a variety of internal, presumably genetic and inherited, factors. The viral theory of cancer and leukemia was in disrepute. During those early years only a few tumors, such as chicken leukemia, chicken sarcoma, mouse mammary carcinoma, frogkidney carcinoma and some of the warts and papillomas in rabbits, dogs, cattle and human beings, were found to be transmissible by filtrates and were therefore believed to be caused by filterable viruses.1 , 2 Gradually, experimental tools became available, among them pedigreed strains of mice, propagation of . . .

Viruses Attacking the Honey Bee

Publisher Summary Honey bee viruses possess small unenclosed particles containing ribonucleic acid (RNA). Each known type of virus native to bees may represent a group of related but distinguishable strains that differ in certain ways, including their virulence for any one strain of bee. Different virus strains may also vary in host range. Two of the diseases of bees caused by viruses have been recognized since the beginning of the century. One of them is sacbrood of the larval bee that is caused by a “filterable virus” and was one of the first virus diseases to be identified in insects. The second disease, paralysis of the adult bee, is caused by a filterable virus, but the agents causing these diseases were identified until much later. This chapter describes the methods of identification, properties, virus multiplication, and spread of infection of several honey bee virus. These viruses include sacbrood virus, chronic bee-paralysis virus, acute bee-paralysis virus, Arkansas bee virus, bee virus X, slow-paralysis virus, and Nodamura virus. Several other possible bee viruses such as particles associated with “Shiny-Black” disease and a possible satellite virus are also described in the chapter. The mechanisms that prevent the viruses from multiplying and attacking may differ in the host.