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“Unprecedented detail” was observed about how a patient’s clinical condition changes in response to Ebola virus disease and treatment. That’s what NIH researchers who analyzed daily gene activation found in a 26-day study of 1 patient.
The patient, who was admitted to the NIH Clinical Center on day 7 of illness, received intensive supportive care, including fluids and electrolytes, but did not receive any experimental Ebola drugs. The researchers took blood samples daily to measure the rise and decline of virus replication and to track the timing, intensity, and duration of expression of numerous immune system genes. They correlated changes in gene expression with subsequent alterations in the patient’s clinical condition, such as development and resolution of blood-clotting dysfunction.
The researchers pinpointed “key transition points” in the response to infection, NIH says. For example, they observed a marked decline in antiviral responses that correlated with clearance of virus from white blood cells. The researchers also found that most host responses shifted rapidly from activating genes involved in cell damage and inflammation toward those linked to promotion of cellular and organ repair—a “pivot” that came before the patient began showing signs of clinical improvement.
Although the study centered on only 1 patient, the researchers say it may help inform the development of treatments designed to boost or accelerate host factors that counter the virus and promote healing.
“Unprecedented detail” was observed about how a patient’s clinical condition changes in response to Ebola virus disease and treatment. That’s what NIH researchers who analyzed daily gene activation found in a 26-day study of 1 patient.
The patient, who was admitted to the NIH Clinical Center on day 7 of illness, received intensive supportive care, including fluids and electrolytes, but did not receive any experimental Ebola drugs. The researchers took blood samples daily to measure the rise and decline of virus replication and to track the timing, intensity, and duration of expression of numerous immune system genes. They correlated changes in gene expression with subsequent alterations in the patient’s clinical condition, such as development and resolution of blood-clotting dysfunction.
The researchers pinpointed “key transition points” in the response to infection, NIH says. For example, they observed a marked decline in antiviral responses that correlated with clearance of virus from white blood cells. The researchers also found that most host responses shifted rapidly from activating genes involved in cell damage and inflammation toward those linked to promotion of cellular and organ repair—a “pivot” that came before the patient began showing signs of clinical improvement.
Although the study centered on only 1 patient, the researchers say it may help inform the development of treatments designed to boost or accelerate host factors that counter the virus and promote healing.
“Unprecedented detail” was observed about how a patient’s clinical condition changes in response to Ebola virus disease and treatment. That’s what NIH researchers who analyzed daily gene activation found in a 26-day study of 1 patient.
The patient, who was admitted to the NIH Clinical Center on day 7 of illness, received intensive supportive care, including fluids and electrolytes, but did not receive any experimental Ebola drugs. The researchers took blood samples daily to measure the rise and decline of virus replication and to track the timing, intensity, and duration of expression of numerous immune system genes. They correlated changes in gene expression with subsequent alterations in the patient’s clinical condition, such as development and resolution of blood-clotting dysfunction.
The researchers pinpointed “key transition points” in the response to infection, NIH says. For example, they observed a marked decline in antiviral responses that correlated with clearance of virus from white blood cells. The researchers also found that most host responses shifted rapidly from activating genes involved in cell damage and inflammation toward those linked to promotion of cellular and organ repair—a “pivot” that came before the patient began showing signs of clinical improvement.
Although the study centered on only 1 patient, the researchers say it may help inform the development of treatments designed to boost or accelerate host factors that counter the virus and promote healing.