Pub Date : 2016-11-28DOI: 10.15406/jhvrv.2016.04.00127
L. Webber
{"title":"Yellow Fever: The Resurgence of a Forgotten Disease and HIV-Infected Travellers","authors":"L. Webber","doi":"10.15406/jhvrv.2016.04.00127","DOIUrl":"https://doi.org/10.15406/jhvrv.2016.04.00127","url":null,"abstract":"","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2016-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-23DOI: 10.15406/jhvrv.2016.04.00125
G. N. Kim, Kunyu Wu, Hwa‐Yong An, E. Banasikowska, M. Harding, C. Kang
Recently, we developed attenuated VSV vectors by introducing temperature sensitive (ts) mutations in the M gene in both VSV Indiana and New Jersey serotypes. The newly generated M gene mutants of rVSV vectors are rVSVInd(GML) with mutations of G21E, M51R, and L111F, rVSVNJ(GMM) with mutations of G22E, M48R, and M51R, and rVSVNJ(GMML) with mutations of G22E, M48R, M51R, and L110F. Our purpose was to examine the immunogenicity of the new ts M gene mutant of rVSVInd and attenuated M gene mutants ofrVSVNJas vaccine vectors against HIV-1 proteins. We generated attenuated rVSVs carrying HIV-1 gag, pol, and env genes. We immunized mice with various prime-boost vaccination regimens. CD8+ T cell responses and humoral immune responses in the vaccinated mice were examined. Priming with rVSVInd(GML)-gag, pol, or env gene of HIV-1 and boosting with rVSVNJ(GMM)-gag, pol, or env gene or rVSVNJ(GMML)-gag, pol, or env gene induced the strongest CD8+ cytotoxic T cell responses against the HIV-1 Gag, RT, and Env proteins. The same vaccination regimen also induced strong humoral immune responses against the HIV-1 Gag and Env proteins. We conclude that rVSVInd(GML) priming followed by rVSVNJ(GMM) boosting is the best vaccination regimen for optimum B cell and T cell adaptive immune responses against inserted foreign gene products when the newly attenuated rVSVInd and rVSVNJ are used.
{"title":"Matrix Protein Gene Variants of Two Distinct Serotypes of rVSV Make Effective Viral Vectors for Prime-Boost Vaccination","authors":"G. N. Kim, Kunyu Wu, Hwa‐Yong An, E. Banasikowska, M. Harding, C. Kang","doi":"10.15406/jhvrv.2016.04.00125","DOIUrl":"https://doi.org/10.15406/jhvrv.2016.04.00125","url":null,"abstract":"Recently, we developed attenuated VSV vectors by introducing temperature sensitive (ts) mutations in the M gene in both VSV Indiana and New Jersey serotypes. The newly generated M gene mutants of rVSV vectors are rVSVInd(GML) with mutations of G21E, M51R, and L111F, rVSVNJ(GMM) with mutations of G22E, M48R, and M51R, and rVSVNJ(GMML) with mutations of G22E, M48R, M51R, and L110F. Our purpose was to examine the immunogenicity of the new ts M gene mutant of rVSVInd and attenuated M gene mutants ofrVSVNJas vaccine vectors against HIV-1 proteins. We generated attenuated rVSVs carrying HIV-1 gag, pol, and env genes. We immunized mice with various prime-boost vaccination regimens. CD8+ T cell responses and humoral immune responses in the vaccinated mice were examined. Priming with rVSVInd(GML)-gag, pol, or env gene of HIV-1 and boosting with rVSVNJ(GMM)-gag, pol, or env gene or rVSVNJ(GMML)-gag, pol, or env gene induced the strongest CD8+ cytotoxic T cell responses against the HIV-1 Gag, RT, and Env proteins. The same vaccination regimen also induced strong humoral immune responses against the HIV-1 Gag and Env proteins. We conclude that rVSVInd(GML) priming followed by rVSVNJ(GMM) boosting is the best vaccination regimen for optimum B cell and T cell adaptive immune responses against inserted foreign gene products when the newly attenuated rVSVInd and rVSVNJ are used.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2016-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-23DOI: 10.15406/JHVRV.2016.04.00124
W. Martin
{"title":"The ACE Pathway in Comparison to the Immune System in the Defense Against Infectious Diseases","authors":"W. Martin","doi":"10.15406/JHVRV.2016.04.00124","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.04.00124","url":null,"abstract":"","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-11DOI: 10.15406/JHVRV.2016.04.00123
Eloke Onyebuchi
Polio virus is very stable and can remain infectious for relatively long periods in food and water, which are its main route of transmission before it invades the lymph nodes or sometimes enters the bloodstream where it persists to cause viremia. In majority of cases (99%), clinical disease does not result while in minority of cases (1%) enters the central nervous system where it causes paralytic poliomyelitis.
{"title":"Eradicating Polio Menace in Nigeria","authors":"Eloke Onyebuchi","doi":"10.15406/JHVRV.2016.04.00123","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.04.00123","url":null,"abstract":"Polio virus is very stable and can remain infectious for relatively long periods in food and water, which are its main route of transmission before it invades the lymph nodes or sometimes enters the bloodstream where it persists to cause viremia. In majority of cases (99%), clinical disease does not result while in minority of cases (1%) enters the central nervous system where it causes paralytic poliomyelitis.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-09DOI: 10.15406/JHVRV.2016.04.00122
A. Cheepsattayakorn, R. Cheepsattayakorn
{"title":"Novel Antiretroviral Drugs for HIV/AIDS","authors":"A. Cheepsattayakorn, R. Cheepsattayakorn","doi":"10.15406/JHVRV.2016.04.00122","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.04.00122","url":null,"abstract":"","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2016-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-03DOI: 10.15406/JHVRV.2016.04.00121
L. Temoshok
Patient adherence is arguably the most important factor determining both individual and public health benefits of antiretroviral therapy (ART). Adherence issues also appear to be central in understanding the large disparities between African Americans and Whites in terms of lower rates of ART utilization and adherence. In an attempt to understand factors which constitute barriers or facilitators of adherence, particularly in African American populations, seven studies are reviewed which focus on the largely disadvantaged and African American patients receiving HIV care through the University of Maryland Medical System in Baltimore. Analysis of these studies reveals that ART adherence is better understood and predicted by “non-obvious,” complex, and often underlying factors, including the adverse circumstances which describe the HIV-infected individual who ends up receiving care in an emergency room and inpatient setting rather than from the same clinician in an outpatient clinic, patients’ subjective perceptions of their health care providers, mistrustful beliefs about HIV and its treatment, and dimensions of forgiveness and how these affect attitudes and behaviors about being HIV-infected and relating to others, medical systems, and God or spiritual being. More “obvious” factors such as knowledge of HIV and its treatment, “pill burden,” or providing external incentives or methods intended to help patients take their prescribed medicines do not play a significant role in adherence, and moreover, may have counter-intuitive effects, as discussed in two studies. We present a model of biodisparity, as the biological entrenchment of socioeconomic and healthcare access disparities, resulting from the conjoint influence of suboptimal adherence and the transmission of drug resistant virus within isolated social networks and disadvantaged sub-populations.
{"title":"Adherence to Antiretroviral Therapy among Patients Attending an Inner-City HIV Primary Care Clinic: Non-obvious Factors are Most Important","authors":"L. Temoshok","doi":"10.15406/JHVRV.2016.04.00121","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.04.00121","url":null,"abstract":"Patient adherence is arguably the most important factor determining both individual and public health benefits of antiretroviral therapy (ART). Adherence issues also appear to be central in understanding the large disparities between African Americans and Whites in terms of lower rates of ART utilization and adherence. In an attempt to understand factors which constitute barriers or facilitators of adherence, particularly in African American populations, seven studies are reviewed which focus on the largely disadvantaged and African American patients receiving HIV care through the University of Maryland Medical System in Baltimore. Analysis of these studies reveals that ART adherence is better understood and predicted by “non-obvious,” complex, and often underlying factors, including the adverse circumstances which describe the HIV-infected individual who ends up receiving care in an emergency room and inpatient setting rather than from the same clinician in an outpatient clinic, patients’ subjective perceptions of their health care providers, mistrustful beliefs about HIV and its treatment, and dimensions of forgiveness and how these affect attitudes and behaviors about being HIV-infected and relating to others, medical systems, and God or spiritual being. More “obvious” factors such as knowledge of HIV and its treatment, “pill burden,” or providing external incentives or methods intended to help patients take their prescribed medicines do not play a significant role in adherence, and moreover, may have counter-intuitive effects, as discussed in two studies. We present a model of biodisparity, as the biological entrenchment of socioeconomic and healthcare access disparities, resulting from the conjoint influence of suboptimal adherence and the transmission of drug resistant virus within isolated social networks and disadvantaged sub-populations.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-02DOI: 10.15406/JHVRV.2016.04.00120
P. Shanti, Ey, Shardulendra Prasad Sherch, P. Man, Har, N. Pokhrel, A. Globig, S. Sherchan
A serological survey for Avian Influenza Virus (AIV) subtype H5, H7 and H9 antibodies in domestic ducks was carried out in 2009 at Central Veterinary Laboratory (CVL), Kathmandu, Nepal. A total of 1000 serum samples were tested from various localities of 11 districts of Nepal, categorized as to be at high risk for the introduction of Highly Pathogenic Avian Influenza Virus (HPAIV) of H5N1 subtype. Sero-positive result against AIV H5 was found in three districts of eastern region with the highest prevalence (6.28 %) in Jhapa (p< 0.001). Likewise, sero-positive samples against AIV H9 were detected in Chitwan, Kapilbastu, Nawalparasi and Kaski districts. However, none of the samples was found to be sero-positive against AIV H7. All the samples positive against H5 were sampled in December 2008 exclusively (p< 0.001). In contrast, two samples collected before September 2008 and three samples after this time until January 2009 were sero-positive against AIV H9. Our findings indicate higher prevalence of AIV subtype H5 compared to H7 and H9 in duck species of Nepal.
{"title":"Serological Surveillance of Avian Influenza Virus in Nepal","authors":"P. Shanti, Ey, Shardulendra Prasad Sherch, P. Man, Har, N. Pokhrel, A. Globig, S. Sherchan","doi":"10.15406/JHVRV.2016.04.00120","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.04.00120","url":null,"abstract":"A serological survey for Avian Influenza Virus (AIV) subtype H5, H7 and H9 antibodies in domestic ducks was carried out in 2009 at Central Veterinary Laboratory (CVL), Kathmandu, Nepal. A total of 1000 serum samples were tested from various localities of 11 districts of Nepal, categorized as to be at high risk for the introduction of Highly Pathogenic Avian Influenza Virus (HPAIV) of H5N1 subtype. Sero-positive result against AIV H5 was found in three districts of eastern region with the highest prevalence (6.28 %) in Jhapa (p< 0.001). Likewise, sero-positive samples against AIV H9 were detected in Chitwan, Kapilbastu, Nawalparasi and Kaski districts. However, none of the samples was found to be sero-positive against AIV H7. All the samples positive against H5 were sampled in December 2008 exclusively (p< 0.001). In contrast, two samples collected before September 2008 and three samples after this time until January 2009 were sero-positive against AIV H9. Our findings indicate higher prevalence of AIV subtype H5 compared to H7 and H9 in duck species of Nepal.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-01DOI: 10.15406/JHVRV.2016.04.00119
R. Kalkeri
Heterodimeric receptors of the beta1 and beta3 integrin families are shown to play an important role in platelet adhesion and aggregation, which is critical for homeostasis and thrombosis [11]. In particular, GPIIb/IIIa integrant complex on platelets binds to collagen, fibrinogen and Von Willebrand Factor, resulting in platelet activation. This activation triggers the coagulation cascade resulting in blood clot formation and hemorrhage control. Ebola virus glycoprotein’s (GP) are shown to interact with Integrins (beta1) and may be involved in the virus entry. Ebola GP expression also led to the down regulation of integrins [12]. Integrand αV was required for efficient GP-mediated transduction and EBOV infection of macrophages [13]. Binding of Ebola virus GP to aVbIII integrins is also shown to prime the endosomal cathepsins, a necessary step in the Ebola virus entry [14]. VP35 protein (required for viral transcription) of Ebola virus contains RGD (Arg-Gly-Asp) and several RGD like motifs in the Table 1. Interestingly, RGD/KGD peptide motif is a conserved feature of low molecular weight non-enzymatic proteins called as “disinterring” present in snake venoms [15]. These molecules bind to the platelet surface integrins (such as alphaII-beta3), blocking the interaction of the platelets with the natural substrates such as fibrinogen and von Willebrand factor. This blockage results in potential inhibition of platelet aggregation [16] (and thus preventing fibrin clots), a crucial step in homeostasis. Due to the presence of conserved RGD and RGD like motifs in VP35, it is possible that VP35 protein might potentially block/delay platelet aggregation. Delayed platelet aggregation might inhibit blood clotting in response to vascular injury/altered vascular barrier observed in the Ebola virus infected patients, thus exacerbating hemorrhages. Significantly decreased platelet aggregation observed in experimentally infected rhesus macaques supports this theory [17]. Table 1: Arg-Gly-Asp (RGD) and similar motifs present in the VP35 protein of Ebola virus (Accession number AAM76032) with the amino acid residue numbers are shown in the figure. Amino acids are represented by single alphabets according to the standard nomenclature.
{"title":"Does Disruption of Integrins Play a Role on Ebola Virus Hemorrhagic Fever Syndrome","authors":"R. Kalkeri","doi":"10.15406/JHVRV.2016.04.00119","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.04.00119","url":null,"abstract":"Heterodimeric receptors of the beta1 and beta3 integrin families are shown to play an important role in platelet adhesion and aggregation, which is critical for homeostasis and thrombosis [11]. In particular, GPIIb/IIIa integrant complex on platelets binds to collagen, fibrinogen and Von Willebrand Factor, resulting in platelet activation. This activation triggers the coagulation cascade resulting in blood clot formation and hemorrhage control. Ebola virus glycoprotein’s (GP) are shown to interact with Integrins (beta1) and may be involved in the virus entry. Ebola GP expression also led to the down regulation of integrins [12]. Integrand αV was required for efficient GP-mediated transduction and EBOV infection of macrophages [13]. Binding of Ebola virus GP to aVbIII integrins is also shown to prime the endosomal cathepsins, a necessary step in the Ebola virus entry [14]. VP35 protein (required for viral transcription) of Ebola virus contains RGD (Arg-Gly-Asp) and several RGD like motifs in the Table 1. Interestingly, RGD/KGD peptide motif is a conserved feature of low molecular weight non-enzymatic proteins called as “disinterring” present in snake venoms [15]. These molecules bind to the platelet surface integrins (such as alphaII-beta3), blocking the interaction of the platelets with the natural substrates such as fibrinogen and von Willebrand factor. This blockage results in potential inhibition of platelet aggregation [16] (and thus preventing fibrin clots), a crucial step in homeostasis. Due to the presence of conserved RGD and RGD like motifs in VP35, it is possible that VP35 protein might potentially block/delay platelet aggregation. Delayed platelet aggregation might inhibit blood clotting in response to vascular injury/altered vascular barrier observed in the Ebola virus infected patients, thus exacerbating hemorrhages. Significantly decreased platelet aggregation observed in experimentally infected rhesus macaques supports this theory [17]. Table 1: Arg-Gly-Asp (RGD) and similar motifs present in the VP35 protein of Ebola virus (Accession number AAM76032) with the amino acid residue numbers are shown in the figure. Amino acids are represented by single alphabets according to the standard nomenclature.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"57 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-10-20DOI: 10.15406/JHVRV.2016.03.00116
B. Andrić, G. Mijović, Aleks, A. Andric
The Hand, Foot and Mouth Disease (HFMD) are an acute, highly contagious viral disease. Initial symptoms are fever, poor appetite, and fatigue. The fever occurs 1-2 days after onset of oral ulceration. Then on the distal parts of the extremities occurs rash, usually lasts for 7-10 days, and spontaneously resolved. The disease is most often had classified as benign infection, which generally does not require therapeutic treatment. Recent findings have been warning that the number of maladies cases of HFMD in the world is growing. Especially in the last four years, serious cases with many severe complications, (aseptic meningitis, pneumonia, prolonged febrile state, long-term fatigue, muscle and joint pain, recurrent pain, expressed dehydration) increasing. Examination of the major epidemics in the world has shown that the most common causes of diseases are two types of enter viruses (Ev): Coxsakievirus (Cox) of the group A, subtype A16 (CoxA-16), and enter virus 71 (Ev-71). ECHO and other enteroviruses may also be associated with HFMD. In September 2014, in Montenegro were registered epidemic of HFMD with 29 diagnostic cases. In the total sample of maladies, child population of 4-12 years accounted for 20 (71%), and adults for 9 (29%) cases. The first cases were registering in Pljevlja. In short time, disease has assumed epidemic proportions with 25 registered cases. In the same period in Podgorica were registered four cases. We analyzed the epidemiological, clinical characteristics of the disease, with special emphasis on diagnostic difficulties and prognosis of disease.
{"title":"Characteristics of Hand Foot and Mouth Disease","authors":"B. Andrić, G. Mijović, Aleks, A. Andric","doi":"10.15406/JHVRV.2016.03.00116","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.03.00116","url":null,"abstract":"The Hand, Foot and Mouth Disease (HFMD) are an acute, highly contagious viral disease. Initial symptoms are fever, poor appetite, and fatigue. The fever occurs 1-2 days after onset of oral ulceration. Then on the distal parts of the extremities occurs rash, usually lasts for 7-10 days, and spontaneously resolved. The disease is most often had classified as benign infection, which generally does not require therapeutic treatment. \u0000 \u0000 Recent findings have been warning that the number of maladies cases of HFMD in the world is growing. Especially in the last four years, serious cases with many severe complications, (aseptic meningitis, pneumonia, prolonged febrile state, long-term fatigue, muscle and joint pain, recurrent pain, expressed dehydration) increasing. Examination of the major epidemics in the world has shown that the most common causes of diseases are two types of enter viruses (Ev): Coxsakievirus (Cox) of the group A, subtype A16 (CoxA-16), and enter virus 71 (Ev-71). ECHO and other enteroviruses may also be associated with HFMD. \u0000 \u0000 In September 2014, in Montenegro were registered epidemic of HFMD with 29 diagnostic cases. In the total sample of maladies, child population of 4-12 years accounted for 20 (71%), and adults for 9 (29%) cases. The first cases were registering in Pljevlja. In short time, disease has assumed epidemic proportions with 25 registered cases. In the same period in Podgorica were registered four cases. We analyzed the epidemiological, clinical characteristics of the disease, with special emphasis on diagnostic difficulties and prognosis of disease.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"60 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-10-20DOI: 10.15406/JHVRV.2016.03.00117
S. Jeffress, A. Taylor-Robinson
Viral haemorrhagic fevers form a distinctive category of illness in humans that is typically, but not definitively, characterized by internal bleeding and fever. Disease manifestations are attributed to an autoimmune disorder that is triggered by prior exposure to one of several RNA viruses. These include such well known viruses as Ebola and Lassa, the associated fevers for which are often lethal, even with medical intervention, to dengue and Zika, which do cause severe complications but that are also often subclinical. Aside from the pressing need to establish precisely the mechanism of VHF pathogenicity, screening of genetic markers for comorbidity, which are in close proximity on the same human chromosome and thus may be inherited together, should help to determine risk factors for unrelated inheritable diseases and metabolic disorders. An exemplar is the autoimmune condition type 1 diabetes, which has been identified as a risk factor for dengue haemorrhagic fever. Any correlations found between VHF and a disease with a known molecular basis, such as type 1 diabetes, may be investigated further by examining genomic regions close to those associated with the identified condition. This may reveal genes which encode proteins that play a putative role in the pathogenesis of VHF.
{"title":"An Epidemiological Approach to Uncover Comorbidities as Potential Risk Factors for Development of Viral Haemorrhagic Fever","authors":"S. Jeffress, A. Taylor-Robinson","doi":"10.15406/JHVRV.2016.03.00117","DOIUrl":"https://doi.org/10.15406/JHVRV.2016.03.00117","url":null,"abstract":"Viral haemorrhagic fevers form a distinctive category of illness in humans that is typically, but not definitively, characterized by internal bleeding and fever. Disease manifestations are attributed to an autoimmune disorder that is triggered by prior exposure to one of several RNA viruses. These include such well known viruses as Ebola and Lassa, the associated fevers for which are often lethal, even with medical intervention, to dengue and Zika, which do cause severe complications but that are also often subclinical. Aside from the pressing need to establish precisely the mechanism of VHF pathogenicity, screening of genetic markers for comorbidity, which are in close proximity on the same human chromosome and thus may be inherited together, should help to determine risk factors for unrelated inheritable diseases and metabolic disorders. An exemplar is the autoimmune condition type 1 diabetes, which has been identified as a risk factor for dengue haemorrhagic fever. Any correlations found between VHF and a disease with a known molecular basis, such as type 1 diabetes, may be investigated further by examining genomic regions close to those associated with the identified condition. This may reveal genes which encode proteins that play a putative role in the pathogenesis of VHF.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67075775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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