Journal articles: 'Viral disease'

1

Severson, Jessica L., and Stephen K. Tyring. "Viral disease update." Current Problems in Dermatology 11, no. 2 (March 1999): 37–70. http://dx.doi.org/10.1016/s1040-0486(99)90007-8.

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Stovin, P. "Viral Heart Disease." Journal of Clinical Pathology 38, no. 3 (March 1, 1985): 358. http://dx.doi.org/10.1136/jcp.38.3.358-b.

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Montague, Terrence J., Gary D. Lopaschuk, and Norman J. Davies. "Viral Heart Disease." Chest 98, no. 1 (July 1990): 190–99. http://dx.doi.org/10.1378/chest.98.1.190.

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Gulbahce, Natali, Han Yan, Marc Vidal, and Albert-Laszlo Barabasi. "Viral Disease Networks." Biophysical Journal 98, no. 3 (January 2010): 196a. http://dx.doi.org/10.1016/j.bpj.2009.12.1040.

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Billiau, A. "Viral heart disease." Antiviral Research 5, no. 1 (February 1985): 63. http://dx.doi.org/10.1016/0166-3542(85)90019-1.

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TAPPER, M. L. "Emerging viral diseases and infectious disease risks." Haemophilia 12, s1 (March 2006): 3–7. http://dx.doi.org/10.1111/j.1365-2516.2006.01194.x.

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Franchini, Genoveffa, Richard F. Ambinder, and Michèle Barry. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation.v2000.1.409.20000409.

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As part of the international outreach of the American Society of Hematology, this review addresses some aspects of the genetics, biology, epidemiology, and clinical relevance of viruses that cause a variety of hematopoietic disorders in human populations. The viruses described here have a different pattern of geographical distribution, and the disease manifestations may vary according to environmental and/or genetic characteristics of the host. Epstein-Barr virus, a linear double-stranded DNA virus (herpesvirus), and the human T-cell leukemia virus, a retrovirus with a single-stranded diploid RNA genome, are associated among other diseases with lymphoma and leukemia/lymphoma, respectively. Both viruses cause a lifelong infection, but only a small percentage of infected individuals develop hematopoietic neoplasms. Epidemiological data suggest that the time of infection may be important in determining disease outcome in both HTLV-I and EBV infection. The pathogenic mechanisms used by these viruses are of most interest since they may recapitulate growth dysregulation steps also occurring in other hematopoietic malignancies.In Section I Dr. Franchini reviews the biology, genetics and diseases associated with HTLV-I and HTLV-II. In Section II, Dr. Ambinder reviews the biology of EBV infection and its relationship to the pathogenesis of Hodgkin's disease and other malignancies.In Section III, Dr. Barry reviews the viral hemorrhagic fevers caused by RNA viruses such as Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae, which can lead to acute syndromes that can be fatal. However, prompt diagnosis is key for patient management as well as for limiting their spread to others. These syndromes have become the focus of public concern and represent not only a clinical challenge, since in most cases no specific antiviral treatment is available, but also a challenge for future basic research on their biology and pathogenesis since little is known at present.

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Franchini, Genoveffa, Richard F. Ambinder, and Michèle Barry. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation.v2000.1.409.409.

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Abstract As part of the international outreach of the American Society of Hematology, this review addresses some aspects of the genetics, biology, epidemiology, and clinical relevance of viruses that cause a variety of hematopoietic disorders in human populations. The viruses described here have a different pattern of geographical distribution, and the disease manifestations may vary according to environmental and/or genetic characteristics of the host. Epstein-Barr virus, a linear double-stranded DNA virus (herpesvirus), and the human T-cell leukemia virus, a retrovirus with a single-stranded diploid RNA genome, are associated among other diseases with lymphoma and leukemia/lymphoma, respectively. Both viruses cause a lifelong infection, but only a small percentage of infected individuals develop hematopoietic neoplasms. Epidemiological data suggest that the time of infection may be important in determining disease outcome in both HTLV-I and EBV infection. The pathogenic mechanisms used by these viruses are of most interest since they may recapitulate growth dysregulation steps also occurring in other hematopoietic malignancies. In Section I Dr. Franchini reviews the biology, genetics and diseases associated with HTLV-I and HTLV-II. In Section II, Dr. Ambinder reviews the biology of EBV infection and its relationship to the pathogenesis of Hodgkin's disease and other malignancies. In Section III, Dr. Barry reviews the viral hemorrhagic fevers caused by RNA viruses such as Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae, which can lead to acute syndromes that can be fatal. However, prompt diagnosis is key for patient management as well as for limiting their spread to others. These syndromes have become the focus of public concern and represent not only a clinical challenge, since in most cases no specific antiviral treatment is available, but also a challenge for future basic research on their biology and pathogenesis since little is known at present.

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9

Burgart, L. J. "Cholangitis in viral disease." Mayo Clinic Proceedings 73, no. 5 (May 1, 1998): 479–82. http://dx.doi.org/10.4065/73.5.479.

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10

Liesegang, Thomas J. "Varicella Zoster Viral Disease." Mayo Clinic Proceedings 74, no. 10 (October 1999): 983–98. http://dx.doi.org/10.4065/74.10.983.

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Franchini, G. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation-2000.1.409.

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12

J Buchmeier, Michael, and Thomas E Lane. "Viral-induced neurodegenerative disease." Current Opinion in Microbiology 2, no. 4 (August 1999): 398–402. http://dx.doi.org/10.1016/s1369-5274(99)80070-8.

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Burgart, Lawrence J. "Cholangitis in Viral Disease." Mayo Clinic Proceedings 73, no. 5 (May 1998): 479–82. http://dx.doi.org/10.1016/s0025-6196(11)63735-x.

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14

Liesegang, Thomas J. "Varicella Zoster Viral Disease." Mayo Clinic Proceedings 74, no. 10 (October 1999): 983–98. http://dx.doi.org/10.1016/s0025-6196(11)63996-7.

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15

Capeau, Jacqueline, Lawrence Serfaty, and Mostafa Badr. "PPARs in Viral Disease." PPAR Research 2009 (2009): 1–2. http://dx.doi.org/10.1155/2009/393408.

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16

Vasconcelos, Pedro FC. "Diagnosis of viral disease." Lancet 361, no. 9369 (May 2003): 1589. http://dx.doi.org/10.1016/s0140-6736(03)13307-7.

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17

Weber, T., P. Kennedy, and M. Oette. "Viral neuropathogenesis/Prion disease." Journal of Neurovirology 8, no. 3 (January 2002): 105–13. http://dx.doi.org/10.1080/13550280290100662.

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18

Friedland, J. S. "Chemokines in viral disease." Research in Virology 147, no. 2-3 (March 1996): 131–38. http://dx.doi.org/10.1016/0923-2516(96)80227-5.

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19

Anderson, Monique R., Fatah Kashanchi, and Steven Jacobson. "Exosomes in Viral Disease." Neurotherapeutics 13, no. 3 (June 20, 2016): 535–46. http://dx.doi.org/10.1007/s13311-016-0450-6.

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20

Donnelly, Thomas M. "Emerging viral diseases of rabbits and rodents: Viral hemorrhagic disease and hantavirus infection." Seminars in Avian and Exotic Pet Medicine 4, no. 2 (April 1995): 83–91. http://dx.doi.org/10.1016/s1055-937x(05)80043-x.

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21

Glick, E., Y. Levy, and Y. Gafni. "The viral etiology of tomato yellow leaf curl disease – a review." Plant Protection Science 45, No. 3 (October 16, 2009): 81–97. http://dx.doi.org/10.17221/26/2009-pps.

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Tomato yellow leaf curl disease (TYLCD) is one of the most devastating plant diseases in the world. As a result of its continuing rapid spread, it now afflicts more than 30 tomato growing countries in the Mediterranean basin, southern Asia, Africa, and South, Central and North America. The disease is caused by a group of viral species of the genus Begomovirus, family Geminiviridae (geminiviruses), referred to as Tomato yellow leaf curl virus (TYLCV). These are transmitted by an insect vector, the whitefly Bemisia tabaci, classified in the family Aleyrodidae. The genome of TYLCV generally consists of a single circular single-stranded (ss) DNA molecule, with only one exception in which two components were identified. It encodes six open reading frames, only one of which codes for the coat protein (CP) that represents a building block of the viral particle. TYLCV, like all other members of the Geminiviridae, has geminate particles, apparently consisting of two incomplete T = 1 icosahedra joined together to produce a structure with 22 pentameric capsomers and 110 identical CP subunits. Close to 50 years of intensive research into TYLCV epidemics has been conducted to find solutions to the severe problem caused by this virus. To date, breeding for resistance appears to be the best approach to controlling this disease, although only partially resistant varieties are commercially available. Since the virus consists of a ssDNA that replicates in the host-cell nucleus, the molecular mechanisms involved in its nuclear import have been the focus of our studies in recent years and results, as well as prospects, are discussed in this review. In addition, we describe our recent finding of a suppressor of gene silencing encoded by one of the TYLCV-Isr genes. This paper provides an overview of the most outstanding achievements in TYLCV research that may lead to more effective control strategies.

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22

M, Mr Keshava Reddy, and Mr Senthil Thirusangu. "Viral Hepatitis – Disease Burden, Challenges and Gap Analysis with Existing Response." International Journal of Trend in Scientific Research and Development Volume-3, Issue-3 (April 30, 2019): 545–47. http://dx.doi.org/10.31142/ijtsrd22823.

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23

Braselton, James P., and Martha L. Abell. "A Viral Disease That Damages the Immunity Conferred by Different Viral Diseases or Vaccination." Mathematics 9, no. 8 (April 8, 2021): 808. http://dx.doi.org/10.3390/math9080808.

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In this paper we modify a standard SIR model used to study the spread of some diseases by incorporating a disease that destroys the immunity that is conferred by having one of the other diseases or being vaccinated against the disease. A specific biological example of this occurs with measles. Studies of recent measles’ patients has shown that many patients have lost some (or all) of their immunity to other diseases from which they were previously protected. In the future, models like those developed here might be helpful in understanding how viruses that affect multiple organ systems can impact the effect the disease has on at risk populations.

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24

Ahmed, Jamal Uddin, Muhammad Abdur Rahim, and Khwaja Nazim Uddin. "Emerging Viral Diseases." BIRDEM Medical Journal 7, no. 3 (August 30, 2017): 224–32. http://dx.doi.org/10.3329/birdem.v7i3.33785.

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Human life is intricately related to its surrounding environment which also harbors other animals and some deadly infectious pathogens. Any threat to the environment can thus increase the threat of new and so-called emerging infectious diseases (EIDs) especially novel viral infections called emerging viral diseases. This occurs partly due to changing climate as well as human interference with nature and animal life. An important event in new disease emergence is genetic changes in the pathogen that make it possible to become established in a new host species, productively infect new individuals in the new hosts (typically humans) and create local, regional or worldwide health threats. The world has witnessed some emerging and deadly viral threats in recent past with huge mortality and morbidity. Among them were severe acute respiratory syndrome (SARS), bird flu, swine flu, Middle East respiratory syndrome (MERS), ebola virus disease. Moreover some disease has caused great concern in certain regions including Bangladesh in terms of morbidity, like Nipah virus, Zika virus, Dengue and Chikungunya fever. Here in this article an attempt was made to briefly describe some of these emerging viral infections.Birdem Med J 2017; 7(3): 224-232

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25

Y, Nesradin. "Update on Veterinary Viral Vaccines: A Review." Open Access Journal of Veterinary Science & Research 3, no. 3 (2018): 1–12. http://dx.doi.org/10.23880/oajvsr-16000163.

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Vaccine has made a very significant impact on the control of viral diseases in both humans and animal species. Worldwide eradication of small pox and rinderpest an d drastic reduction in other infection disease are confirming to the fact that vaccination is the most feasible and cost effective strategy for prevention, control and eradication of infectious disease. Veterinary science has made a significant contributio n to the field of vaccine research and development. Among the numerous of infectious diseases in animals, those of viral etiology account for a high burden of cases and they are the most relevant from a veterinary perspective. So, vaccination is the most f easible means that has to be implemented for controlling and eradicating these diseases. The viral vaccines used in veterinary medicine generally categorized into 1 of 3 categories: inactivated vaccines (in which antigens are typically combined with adjuva nts); live attenuated vaccines; and recombinant technology vaccines, which may include subunit antigens or genetically engineered organisms. The majority of vaccines available today rely either on attenuation (weakening) techniques or inactivated (killed) forms of the infectious agent. Even though many vaccines are available and vaccine producing technologies are existed, several viral disease s have no vaccines yet and there are also limitations even on existing vaccines. Therefore, the objective of this seminar paper is to overview the development of veterinary viral vaccines and challenges and opportunities existing in the process of its deve lopment. To be profitable from the veterinary viral vaccines the challenging factors for the development of the vaccines should be managed. In addition, the novel vaccine technologies should be encouraged because they can fill the limitations of convention al live and killed vaccines.

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26

Frölich, K. "Viral diseases of northern ungulates." Rangifer 20, no. 2-3 (March 1, 2000): 83. http://dx.doi.org/10.7557/2.20.2-3.1505.

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This paper describes viral diseases reported in northern ungulates and those that are a potential threat to these species. The following diseases are discussed: bovine viral diarrhoea/mucosal disease (BVD/MD), alphaherpesvirus infections, malignant catarrhal fever (MCF), poxvirus infections, parainfluenza type 3 virus infection, Alvsborg disease, foot-and-mouth disease, epizootic haemorrhage disease of deer and bluetongue disease, rabies, respiratory syncytial virus infection, adenovirus infection, hog-cholera, Aujeszky's disease and equine herpesvirus infections. There are no significant differences in antibody prevalence to BVDV among deer in habitats with high, intermediate and low density of cattle. In addition, sequence analysis from the BVDV isolated from roe deer (Capreolus capreolus) showed that this strain was unique within BVDV group I. Distinct BVDV strains might circulate in free-ranging roe deer populations in Germany and virus transmission may be independent of domestic livestock. Similar results have been obtained in a serological survey of alpha-herpesviruses in deer in Germany. Malignant catarrhal fever was studied in fallow deer (Cervus dama) in Germany: the seroprevalence and positive PCR results detected in sheep originating from the same area as the antibody-positive deer might indicate that sheep are the main reservoir animals. Contagious ecthyma (CE) is a common disease in domestic sheep and goats caused by the orf virus. CE has been diagnosed in Rocky Mountain bighorn sheep (Ovis canadensis), mountain goats (Oreamnos americanus), Dall sheep (Ovis dalli), chamois (Rupkapra rupi-capra), muskox {Ovibos moschatus) and reindeer (Rangifer tarandus). Most parainfluenza type 3 virus infections are mild or clinically undetectable. Serological surveys in wildlife have been successfully conducted in many species. In 1985, a new disease was identified in Swedish moose (Alces alces), designated as Alvsborg disease. This wasting syndrome probably has a multi-factorial etiology. Foot-and-mouth disease virus (FMDV) can infect deer and many other wild artiodactyls. Moose, roe deer and the saiga antelope (Saiga tatarica) are the main hosts of FMDV in the Russian Federation. In addition, serological evidence of a FMD infection without clinical disease was detected in red deer in France. Epizootic haemorrhage disease of deer (EHD) and bluetongue (BT) are acute non-contagious viral diseases of wild ruminants characterised by extensive haemorrhage. Culicoides insects are the main vectors. EHD and BT only play a minor role in Europe but both diseases are widespread in North America.

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27

CLIVER, DEAN O. "Epidemiology of Viral Foodborne Disease." Journal of Food Protection 57, no. 3 (March 1, 1994): 263–66. http://dx.doi.org/10.4315/0362-028x-57.3.263.

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Virus transmission via foods begins with fecal shedding of viruses by humans. Foodborne viruses infect perorally: These same agents have alterative fecal-oral routes, including person- to-person transmission and the water vehicle. No zoonotic viruses are transmitted via foods in North America. Viruses rank high among foodborne disease agents in the United States, even though observation, diagnosis, and reporting of foodborne viral disease are inefficient. Risk assessment in developed countries considers viral infection rates and personal hygiene of food handlers, as well as the opportunities for contamination of shellfish and other foods by untreated sewage. Licensing of a vaccine against hepatitis A that could be administered to food handlers in North America would provide an important means of preventing foodborne viral disease. However, the most general concern in preventing all foodborne viral disease is to keep all human fecal contamination out of food.

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28

Greenberg, Harry B., and Pedro A. Piedra. "Immunization Against Viral Respiratory Disease." Pediatric Infectious Disease Journal 23, Supplement (November 2004): S254—S261. http://dx.doi.org/10.1097/01.inf.0000144756.69887.f8.

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29

von Lichtenberg, Franz. "Viral Hepatitis and Liver Disease." American Journal of Tropical Medicine and Hygiene 39, no. 4 (October 1, 1988): 417. http://dx.doi.org/10.4269/ajtmh.1988.39.4.tm0390040417a.

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30

Tam, Paul K. H., W. G. V. Quint, and D. Van Velzen. "Hirschsprung's Disease: A Viral Etiology?" Pediatric Pathology 12, no. 6 (January 1992): 807–10. http://dx.doi.org/10.3109/15513819209024237.

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31

Takahashi, Mitsuo, and Tatsuo Yamada. "Viral Etiology for Parkinson's Disease." Japanese Journal of Infectious Diseases 52, no. 3 (August 30, 1999): 89–98. http://dx.doi.org/10.7883/yoken.52.89.

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32

Aterman, K. "Neonatal Hepatitis-A Viral Disease?" Pediatric Pathology 9, no. 3 (January 1989): 243–50. http://dx.doi.org/10.3109/15513818909037729.

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33

Englund, Janet, W. Paul Glezen, and Pedro A. Piedra. "Maternal immunization against viral disease." Vaccine 16, no. 14-15 (August 1998): 1456–63. http://dx.doi.org/10.1016/s0264-410x(98)00108-x.

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34

Longman, Ryan E., and Timothy R. B. Johnson. "Viral Respiratory Disease in Pregnancy." Postgraduate Obstetrics & Gynecology 27, no. 22 (November 2007): 1–6. http://dx.doi.org/10.1097/01.pgo.0000299203.10579.50.

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35

&NA;. "Viral Respiratory Disease in Pregnancy." Postgraduate Obstetrics & Gynecology 27, no. 22 (November 2007): 7–8. http://dx.doi.org/10.1097/01.pgo.0000299204.48697.9c.

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36

Hunt, Summer. "Viral Hepatitis and Parkinson’s Disease." Nursing for Women's Health 21, no. 3 (June 2017): 160. http://dx.doi.org/10.1016/s1751-4851(17)30140-x.

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37

Hudson, Robert J. "Disease Surveillance versus Viral Surveillance." Clinical Infectious Diseases 33, no. 2 (July 15, 2001): 265–66. http://dx.doi.org/10.1086/321822.

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38

Meldrum, K. "Viral haemorrhagic disease of rabbits." Veterinary Record 130, no. 18 (May 2, 1992): 407. http://dx.doi.org/10.1136/vr.130.18.407-a.

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39

Goncharov, G. D. "RUBELLA, A VIRAL FISH DISEASE." Annals of the New York Academy of Sciences 126, no. 1 (December 16, 2006): 598–600. http://dx.doi.org/10.1111/j.1749-6632.1965.tb14305.x.

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40

&NA;. "Effective Drugs Against Viral Disease." Nurse Practitioner 27, no. 8 (August 2002): 46. http://dx.doi.org/10.1097/00006205-200208000-00013.

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41

Black, Benjamin O., Séverine Caluwaerts, and Jay Achar. "Ebola viral disease and pregnancy." Obstetric Medicine 8, no. 3 (September 2015): 108–13. http://dx.doi.org/10.1177/1753495x15597354.

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Ebola viral disease’s interaction with pregnancy is poorly understood and remains a particular challenge for medical and para-medical personnel responding to an outbreak. This review article is written with the benefit of hindsight and experience from the largest recorded Ebola outbreak in history. We have provided a broad overview of the issues that arise for pregnant women and for the professionals treating them during an Ebola outbreak. The discussion focuses on the specifics of Ebola infection in pregnancy and possible management strategies, including the delivery of an infected woman. We have also discussed the wider challenges posed to pregnant women and their carers during an epidemic, including the identification of suspected Ebola-infected pregnant women and the impact of the disease on pre-existing health services. This paper outlines current practices in the field, as well as highlighting the gaps in our knowledge and the paramount need to protect the health-care workers directly involved in the management of pregnant women.

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42

Rovner, Daniel, and Leslie Weiner. "Chronic Viral Disease of Myelin." Seminars in Neurology 5, no. 02 (June 1985): 168–79. http://dx.doi.org/10.1055/s-2008-1041513.

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Smith, M. S. H., and A. J. Wakefield. "Viral Association with Crohn's Disease." Annals of Medicine 25, no. 6 (December 1, 1993): 557–61. http://dx.doi.org/10.1080/07853890.1993.12088584.

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44

Jarrett, Ruth F. "Viral involvement in hodgkin's disease." International Journal of Cell Cloning 10, no. 6 (1992): 315–22. http://dx.doi.org/10.1002/stem.5530100602.

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45

Busse, William W. "Viral infections and allergic disease." Clinical Experimental Allergy 21, s1 (May 1991): 68–71. http://dx.doi.org/10.1111/j.1365-2222.1991.tb01708.x.

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46

Aitken, Celia, and Donald J. Jeffries. "Nosocomial Spread of Viral Disease." Clinical Microbiology Reviews 14, no. 3 (July 1, 2001): 528–46. http://dx.doi.org/10.1128/cmr.14.3.528-546.2001.

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SUMMARY Viruses are important causes of nosocomial infection, but the fact that hospital outbreaks often result from introduction(s) from community-based epidemics, together with the need to initiate specific laboratory testing, means that there are usually insufficient data to allow the monitoring of trends in incidences. The most important defenses against nosocomial transmission of viruses are detailed and continuing education of staff and strict adherence to infection control policies. Protocols must be available to assist in the management of patients with suspected or confirmed viral infection in the health care setting. In this review, we present details on general measures to prevent the spread of viral infection in hospitals and other health care environments. These include principles of accommodation of infected patients and approaches to good hygiene and patient management. They provide detail on individual viral diseases accompanied in each case with specific information on control of the infection and, where appropriate, details of preventive and therapeutic measures. The important areas of nosocomial infection due to blood-borne viruses have been extensively reviewed previously and are summarized here briefly, with citation of selected review articles. Human prion diseases, which present management problems very different from those of viral infection, are not included.

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Sheppard, Haynes W., Michael S. Ascher, and John F. Krowka. "Viral burden and HIV disease." Nature 364, no. 6435 (July 1993): 291. http://dx.doi.org/10.1038/364291a0.

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Fauci, Antony S., Giuseppe Pantaleo, Janet Embretson, and Ashley T. Haase. "Viral burden and HIV disease." Nature 364, no. 6435 (July 1993): 291–92. http://dx.doi.org/10.1038/364291b0.

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Pakpoor, Julia, Alastair Noyce, Raph Goldacre, Marianna Selkihova, Stephen Mullin, Anette Schrag, Andrew Lees, and Michael Goldacre. "Viral hepatitis and Parkinson disease." Neurology 88, no. 17 (March 29, 2017): 1630–33. http://dx.doi.org/10.1212/wnl.0000000000003848.

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Objective:To study associations between viral hepatitis and Parkinson disease (PD).Methods:A retrospective cohort study was done by analyzing linked English National Hospital Episode Statistics and mortality data (1999–2011). Cohorts of individuals with hepatitis B, hepatitis C, autoimmune hepatitis, chronic active hepatitis, and HIV were constructed, and compared to a reference cohort for subsequent rates of PD.Results:The standardized rate ratio (RR) of PD following hepatitis B was 1.76 (95% confidence interval [CI] 1.28–2.37) (p < 0.001), based on 44 observed compared with 25 expected cases. The RR of PD following hepatitis C was 1.51 (95% CI, 1.18–1.9) (p < 0.001), based on 48.5 expected and 73 observed cases. There was no significant association between autoimmune hepatitis, chronic active hepatitis or HIV, and subsequent PD. When including only those episodes of care for PD that occurred first at least 1 year following each exposure condition, the RR for hepatitis B and hepatitis C were 1.82 (1.29–2.5) and 1.43 (1.09–1.84), respectively.Conclusions:We report strong evidence in favor of an elevation of rates of subsequent PD in patients with hepatitis B and hepatitis C. These findings may be explained by factors peculiar to viral hepatitis, but whether it reflects consequences of infection, shared disease mechanisms, or the result of antiviral treatment remains to be elucidated. Further work is needed to confirm this association and to investigate pathophysiologic pathways, potentially advancing etiologic understanding of PD more broadly.

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50

Lou, Kai-Jye. "Going viral in Parkinson's disease." Science-Business eXchange 5, no. 6 (February 2012): 141. http://dx.doi.org/10.1038/scibx.2012.141.

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Journal articles on the topic 'Viral disease'

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