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John D Morrey - One of the best experts on this subject based on the ideXlab platform.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of NeuroVirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barrë syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of neurovirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barre syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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causation of acute flaccid paralysis by myelitis and myositis in enterovirus d68 infected mice deficient in interferon αβ γ receptor deficient mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Arnaud J Van Wettere, Donal G Sinex, Bart E TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
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Causation of Acute Flaccid Paralysis by Myelitis and Myositis in Enterovirus-D68 Infected Mice Deficient in Interferon αβ/γ Receptor Deficient Mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Donal G Sinex, Arnaud J. Van Wettere, E. Bart TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
Katherine Zukor - One of the best experts on this subject based on the ideXlab platform.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of NeuroVirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barrë syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of neurovirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barre syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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causation of acute flaccid paralysis by myelitis and myositis in enterovirus d68 infected mice deficient in interferon αβ γ receptor deficient mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Arnaud J Van Wettere, Donal G Sinex, Bart E TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
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Causation of Acute Flaccid Paralysis by Myelitis and Myositis in Enterovirus-D68 Infected Mice Deficient in Interferon αβ/γ Receptor Deficient Mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Donal G Sinex, Arnaud J. Van Wettere, E. Bart TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
Wissam Al-issawi - One of the best experts on this subject based on the ideXlab platform.
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Neuroschistosomiasis mimicking lower back pain: case report of a rare differential diagnosis in a pediatric patient
Patient Safety in Surgery, 2018Co-Authors: Abdulrahman Hamad Al-abdulwahhab, Abdulaziz Mohammad Al-sharydah, Sari Saleh Al-suhibani, Saeed Ahmad Al-jubran, Ali Khalaf Al-haidey, Abdulkhaliq Ibrahim Al-hifzi, Wissam Al-issawiAbstract:Background Spinal myelitis is an infrequent manifestation of Spinal Cord Infection. It is caused by the Schistosoma species, which are endemic in South America, part of the Middle East, and Africa. Case presentation We report the case of a 13-year-old male adolescent complaining of progressive lower back pain and weakness of the lower extremities for 3 days. Initial magnetic resonance imaging revealed typical transverse myelitis. Subsequently, parasite serology showed a markedly elevated level of Schistosoma antibody titers, and cerebroSpinal fluid analysis yielded normal results. Because of our presumptive diagnosis of neuroschistosomiasis, the patient was prescribed an empirical regimen of an anti-parasitic agent, after which his neurological deficit promptly subsided. The patient was followed for 1 year and showed a complete long-term resolution of symptoms. Conclusions This case highlights the increasing prevalence of neuroschistosomiasis in recent years, particularly in patients with a history of travel to endemic regions. Moreover, the study reports the clinicoradiological features of this enigmatic disorder. This rare occurrence potentiates further studies to address unanswered questions about neuroschistosomiasis.
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Neuroschistosomiasis mimicking lower back pain: case report of a rare differential diagnosis in a pediatric patient.
Patient safety in surgery, 2018Co-Authors: Abdulrahman Hamad Al-abdulwahhab, Abdulaziz Mohammad Al-sharydah, Sari Saleh Al-suhibani, Saeed Ahmad Al-jubran, Ali Khalaf Al-haidey, Abdulkhaliq Ibrahim Al-hifzi, Wissam Al-issawiAbstract:Spinal myelitis is an infrequent manifestation of Spinal Cord Infection. It is caused by the Schistosoma species, which are endemic in South America, part of the Middle East, and Africa. We report the case of a 13-year-old male adolescent complaining of progressive lower back pain and weakness of the lower extremities for 3 days. Initial magnetic resonance imaging revealed typical transverse myelitis. Subsequently, parasite serology showed a markedly elevated level of Schistosoma antibody titers, and cerebroSpinal fluid analysis yielded normal results. Because of our presumptive diagnosis of neuroschistosomiasis, the patient was prescribed an empirical regimen of an anti-parasitic agent, after which his neurological deficit promptly subsided. The patient was followed for 1 year and showed a complete long-term resolution of symptoms. This case highlights the increasing prevalence of neuroschistosomiasis in recent years, particularly in patients with a history of travel to endemic regions. Moreover, the study reports the clinicoradiological features of this enigmatic disorder. This rare occurrence potentiates further studies to address unanswered questions about neuroschistosomiasis.
Hong Wang - One of the best experts on this subject based on the ideXlab platform.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of NeuroVirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barrë syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of neurovirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barre syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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causation of acute flaccid paralysis by myelitis and myositis in enterovirus d68 infected mice deficient in interferon αβ γ receptor deficient mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Arnaud J Van Wettere, Donal G Sinex, Bart E TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
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Causation of Acute Flaccid Paralysis by Myelitis and Myositis in Enterovirus-D68 Infected Mice Deficient in Interferon αβ/γ Receptor Deficient Mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Donal G Sinex, Arnaud J. Van Wettere, E. Bart TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
Venkatraman Siddharthan - One of the best experts on this subject based on the ideXlab platform.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of NeuroVirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barrë syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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Zika virus-induced acute myelitis and motor deficits in adult interferon αβ/γ receptor knockout mice
Journal of neurovirology, 2018Co-Authors: Katherine Zukor, Hong Wang, Venkatraman Siddharthan, Justin G. Julander, John D MorreyAbstract:Zika virus (ZIKV) has received widespread attention because of its effect on the developing fetus. It is becoming apparent, however, that severe neurological sequelae, such as Guillian-Barre syndrome (GBS), myelitis, encephalitis, and seizures can occur after Infection of adults. This study demonstrates that a contemporary strain of ZIKV can widely infect astrocytes and neurons in the brain and Spinal Cord of adult, interferon α/β receptor knockout mice (AG129 strain) and cause progressive hindlimb paralysis, as well as severe seizure-like activity during the acute phase of disease. The severity of hindlimb motor deficits correlated with increased numbers of ZIKV-infected lumbosacral Spinal motor neurons and decreased numbers of Spinal motor neurons. Electrophysiological compound muscle action potential (CMAP) amplitudes in response to stimulation of the lumbosacral Spinal Cord were reduced when obvious motor deficits were present. ZIKV immunoreactivity was high, intense, and obvious in tissue sections of the brain and Spinal Cord. Infection in the brain and Spinal Cord was also associated with astrogliosis as well as T cell and neutrophil infiltration. CMAP and histological analysis indicated that peripheral nerve and muscle functions were intact. Consequently, motor deficits in these circumstances appear to be primarily due to myelitis and possibly encephalitis as opposed to a peripheral neuropathy or a GBS-like syndrome. Thus, acute ZIKV Infection of adult AG129 mice may be a useful model for ZIKV-induced myelitis, encephalitis, and seizure activity.
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causation of acute flaccid paralysis by myelitis and myositis in enterovirus d68 infected mice deficient in interferon αβ γ receptor deficient mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Arnaud J Van Wettere, Donal G Sinex, Bart E TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.
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Causation of Acute Flaccid Paralysis by Myelitis and Myositis in Enterovirus-D68 Infected Mice Deficient in Interferon αβ/γ Receptor Deficient Mice
Viruses, 2018Co-Authors: John D Morrey, Hong Wang, Brett L Hurst, Katherine Zukor, Venkatraman Siddharthan, Donal G Sinex, Arnaud J. Van Wettere, E. Bart TarbetAbstract:Enterovirus D68 (EV-D68) caused a large outbreak in the summer and fall of 2014 in the United States. It causes serious respiratory disease, but causation of associated paralysis is controversial, because the virus is not routinely identified in cerebroSpinal fluid. To establish clinical correlates with human disease, we evaluated EV-D68 Infection in non-lethal paralysis mouse models. Ten-day-old mice lacking interferon responses were injected intraperitoneally with the virus. Paralysis developed in hindlimbs. After six weeks of paralysis, the motor neurons were depleted due to viral Infection. Hindlimb muscles were also infected and degenerating. Even at the earliest stage of paralysis, muscles were still infected and were degenerating, in addition to presence of virus in the Spinal Cord. To model natural respiratory Infection, five-day-old mice were infected intranasally with EV-D68. Two of the four infected mice developed forelimb paralysis. The affected limbs had muscle disease, but no Spinal Cord Infection was detected. The unique contributions of this study are that EV-D68 causes paralysis in mice, and that causation by muscle disease, with or without Spinal Cord disease, may help to resolve the controversy that the virus can cause paralysis, even if it cannot be identified in cerebroSpinal fluid.