Herpes simplex virus 1 infection and valacyclovir treatment in schizophrenia: Results from the VISTA study
Several studies have implicated herpes simplex virus-type 1 (HSV-1) in the pathophysiology of schizophrenia. A recent trial demonstrated that the anti-viral medication valacylovir, which prevents replication of activated HSV-1, improved selected cognitive deficits in people with schizophrenia. In th...
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| Published in | Schizophrenia research Vol. 206; pp. 291 - 299 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , |
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| Language | English |
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Elsevier B.V
01.04.2019
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| Abstract | Several studies have implicated herpes simplex virus-type 1 (HSV-1) in the pathophysiology of schizophrenia. A recent trial demonstrated that the anti-viral medication valacylovir, which prevents replication of activated HSV-1, improved selected cognitive deficits in people with schizophrenia. In this study, we examined demographic and illness related differences between HSV-1 positive versus HSV-1 negative subjects with early phase schizophrenia and attempted to replicate the previous valacyclovir treatment results in this population.
170 subjects with schizophrenia (HSV-1 positive N = 70; HSV-1 negative N = 96) from 12 US sites participated in the HSV-1 positive versus negative comparisons, and were randomized 1:1 to valacyclovir (1.5 g BID) or placebo for a 16-week, double-blind efficacy trial. The primary endpoints were working and verbal memory.
The HSV-1 positive group, as compared to the HSV-1 negative group, were older (p < 0.001) with fewer males (p = 0.003), and had a longer duration of illness (p = 0.008), more positive symptoms (p = 0.013), poorer quality of life (p = 0.034) and more impairment on the letter-number sequencing test, which is a measure of working memory (p = 0.045). Valacyclovir failed to significantly improve any of the cognitive indices, symptom or functioning measures.
HSV-1 sero-positivity appears to be a marker of a subgroup with a more severe form of schizophrenia. Valacyclovir was not efficacious in the study, perhaps because the herpes virus was in the dormant, non-activated state and therefore non-responsive to valacyclovir effects.
ClinicalTrials.gov Identifier: NCT02008773 |
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| AbstractList | Several studies have implicated herpes simplex virus-type 1 (HSV-1) in the pathophysiology of schizophrenia. A recent trial demonstrated that the anti-viral medication valacylovir, which prevents replication of activated HSV-1, improved selected cognitive deficits in people with schizophrenia. In this study, we examined demographic and illness related differences between HSV-1 positive versus HSV-1 negative subjects with early phase schizophrenia and attempted to replicate the previous valacyclovir treatment results in this population.
170 subjects with schizophrenia (HSV-1 positive N = 70; HSV-1 negative N = 96) from 12 US sites participated in the HSV-1 positive versus negative comparisons, and were randomized 1:1 to valacyclovir (1.5 g BID) or placebo for a 16-week, double-blind efficacy trial. The primary endpoints were working and verbal memory.
The HSV-1 positive group, as compared to the HSV-1 negative group, were older (p < 0.001) with fewer males (p = 0.003), and had a longer duration of illness (p = 0.008), more positive symptoms (p = 0.013), poorer quality of life (p = 0.034) and more impairment on the letter-number sequencing test, which is a measure of working memory (p = 0.045). Valacyclovir failed to significantly improve any of the cognitive indices, symptom or functioning measures.
HSV-1 sero-positivity appears to be a marker of a subgroup with a more severe form of schizophrenia. Valacyclovir was not efficacious in the study, perhaps because the herpes virus was in the dormant, non-activated state and therefore non-responsive to valacyclovir effects.
ClinicalTrials.gov Identifier: NCT02008773 Several studies have implicated herpes simplex virus-type 1 (HSV-1) in the pathophysiology of schizophrenia. A recent trial demonstrated that the anti-viral medication valacylovir, which prevents replication of activated HSV-1, improved selected cognitive deficits in people with schizophrenia. In this study, we examined demographic and illness related differences between HSV-1 positive versus HSV-1 negative subjects with early phase schizophrenia and attempted to replicate the previous valacyclovir treatment results in this population. 170 subjects with schizophrenia (HSV-1 positive N = 70; HSV-1 negative N = 96) from 12 US sites participated in the HSV-1 positive versus negative comparisons, and were randomized 1:1 to valacyclovir (1.5 g BID) or placebo for a 16-week, double-blind efficacy trial. The primary endpoints were working and verbal memory. The HSV-1 positive group, as compared to the HSV-1 negative group, were older (p < 0.001) with fewer males (p = 0.003), and had a longer duration of illness (p = 0.008), more positive symptoms (p = 0.013), poorer quality of life (p = 0.034) and more impairment on the letter-number sequencing test, which is a measure of working memory (p = 0.045). Valacyclovir failed to significantly improve any of the cognitive indices, symptom or functioning measures. HSV-1 sero-positivity appears to be a marker of a subgroup with a more severe form of schizophrenia. Valacyclovir was not efficacious in the study, perhaps because the herpes virus was in the dormant, non-activated state and therefore non-responsive to valacyclovir effects. ClinicalTrials.gov Identifier: NCT02008773. Several studies have implicated herpes simplex virus-type 1 (HSV-1) in the pathophysiology of schizophrenia. A recent trial demonstrated that the anti-viral medication valacylovir, which prevents replication of activated HSV-1, improved selected cognitive deficits in people with schizophrenia. In this study, we examined demographic and illness related differences between HSV-1 positive versus HSV-1 negative subjects with early phase schizophrenia and attempted to replicate the previous valacyclovir treatment results in this population.BACKGROUNDSeveral studies have implicated herpes simplex virus-type 1 (HSV-1) in the pathophysiology of schizophrenia. A recent trial demonstrated that the anti-viral medication valacylovir, which prevents replication of activated HSV-1, improved selected cognitive deficits in people with schizophrenia. In this study, we examined demographic and illness related differences between HSV-1 positive versus HSV-1 negative subjects with early phase schizophrenia and attempted to replicate the previous valacyclovir treatment results in this population.170 subjects with schizophrenia (HSV-1 positive N = 70; HSV-1 negative N = 96) from 12 US sites participated in the HSV-1 positive versus negative comparisons, and were randomized 1:1 to valacyclovir (1.5 g BID) or placebo for a 16-week, double-blind efficacy trial. The primary endpoints were working and verbal memory.METHODS170 subjects with schizophrenia (HSV-1 positive N = 70; HSV-1 negative N = 96) from 12 US sites participated in the HSV-1 positive versus negative comparisons, and were randomized 1:1 to valacyclovir (1.5 g BID) or placebo for a 16-week, double-blind efficacy trial. The primary endpoints were working and verbal memory.The HSV-1 positive group, as compared to the HSV-1 negative group, were older (p < 0.001) with fewer males (p = 0.003), and had a longer duration of illness (p = 0.008), more positive symptoms (p = 0.013), poorer quality of life (p = 0.034) and more impairment on the letter-number sequencing test, which is a measure of working memory (p = 0.045). Valacyclovir failed to significantly improve any of the cognitive indices, symptom or functioning measures.RESULTSThe HSV-1 positive group, as compared to the HSV-1 negative group, were older (p < 0.001) with fewer males (p = 0.003), and had a longer duration of illness (p = 0.008), more positive symptoms (p = 0.013), poorer quality of life (p = 0.034) and more impairment on the letter-number sequencing test, which is a measure of working memory (p = 0.045). Valacyclovir failed to significantly improve any of the cognitive indices, symptom or functioning measures.HSV-1 sero-positivity appears to be a marker of a subgroup with a more severe form of schizophrenia. Valacyclovir was not efficacious in the study, perhaps because the herpes virus was in the dormant, non-activated state and therefore non-responsive to valacyclovir effects. ClinicalTrials.gov Identifier: NCT02008773.CONCLUSIONSHSV-1 sero-positivity appears to be a marker of a subgroup with a more severe form of schizophrenia. Valacyclovir was not efficacious in the study, perhaps because the herpes virus was in the dormant, non-activated state and therefore non-responsive to valacyclovir effects. ClinicalTrials.gov Identifier: NCT02008773. |
| Author | Dickerson, Faith B. Hoffmeyer, Debra Marder, Stephen Macaluso, Matthew Yolken, Robert H. Vohs, Jenifer L. Maguire, Gerald D'Souza, Deepak Highum, Diane Mehdiyoun, Nicole Radnovich, Alexander Kakar, Rishi Wurfel, Brent Dunn, Walter Metzler, Emmalee Yang, Ziyi Nuechterlein, Keith Breier, Alan Coskinas, Evagelos Francis, Michael M. Buchanan, Robert W. Preskorn, Sheldon Zhang, Ying Litman, Robert Visco, Andrew |
| Author_xml | – sequence: 1 givenname: Alan surname: Breier fullname: Breier, Alan email: abreier@iupui.edu organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 2 givenname: Robert W. surname: Buchanan fullname: Buchanan, Robert W. organization: Maryland Psychiatric Research Center, University of Maryland, Baltimore, MD, United States of America – sequence: 3 givenname: Deepak surname: D'Souza fullname: D'Souza, Deepak organization: Yale University School of Medicine, New Haven, CT, United States of America – sequence: 4 givenname: Keith orcidid: 0000-0002-8179-8952 surname: Nuechterlein fullname: Nuechterlein, Keith organization: Semel Institute, UCLA, Los Angeles, CA, United States of America – sequence: 5 givenname: Stephen surname: Marder fullname: Marder, Stephen organization: Semel Institute, UCLA, Los Angeles, CA, United States of America – sequence: 6 givenname: Walter surname: Dunn fullname: Dunn, Walter organization: Semel Institute, UCLA, Los Angeles, CA, United States of America – sequence: 7 givenname: Sheldon surname: Preskorn fullname: Preskorn, Sheldon organization: Kansas University School of Medicine, Wichita, KS, United States of America – sequence: 8 givenname: Matthew surname: Macaluso fullname: Macaluso, Matthew organization: Kansas University School of Medicine, Wichita, KS, United States of America – sequence: 9 givenname: Brent surname: Wurfel fullname: Wurfel, Brent organization: Laureate Institute for Brain Research, KS, United States of America – sequence: 10 givenname: Gerald surname: Maguire fullname: Maguire, Gerald organization: University of California, Riverside, CA, United States of America – sequence: 11 givenname: Rishi surname: Kakar fullname: Kakar, Rishi organization: Segal Institute for Clinical Research, United States of America – sequence: 12 givenname: Diane surname: Highum fullname: Highum, Diane organization: CITrials, Bellflower, CA, United States of America – sequence: 13 givenname: Debra surname: Hoffmeyer fullname: Hoffmeyer, Debra organization: CITrials, Bellflower, CA, United States of America – sequence: 14 givenname: Evagelos surname: Coskinas fullname: Coskinas, Evagelos organization: CITrials, Santa Ana, CA, United States of America – sequence: 15 givenname: Robert surname: Litman fullname: Litman, Robert organization: CBH Health, Rockville, MD, United States of America – sequence: 16 givenname: Jenifer L. surname: Vohs fullname: Vohs, Jenifer L. organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 17 givenname: Alexander surname: Radnovich fullname: Radnovich, Alexander organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 18 givenname: Michael M. surname: Francis fullname: Francis, Michael M. organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 19 givenname: Emmalee surname: Metzler fullname: Metzler, Emmalee organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 20 givenname: Andrew surname: Visco fullname: Visco, Andrew organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 21 givenname: Nicole surname: Mehdiyoun fullname: Mehdiyoun, Nicole organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 22 givenname: Ziyi surname: Yang fullname: Yang, Ziyi organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 23 givenname: Ying surname: Zhang fullname: Zhang, Ying organization: Indiana University School of Medicine, Indianapolis, IN, United States of America – sequence: 24 givenname: Robert H. surname: Yolken fullname: Yolken, Robert H. organization: Johns Hopkins University School of Medicine, Baltimore, MD, United States of America – sequence: 25 givenname: Faith B. surname: Dickerson fullname: Dickerson, Faith B. organization: Sheppard Pratt Health System, Baltimore, MD, United States of America |
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| Keywords | Schizophrenia Cognition Valacyclovir Herpes simplex virus-1 |
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| Title | Herpes simplex virus 1 infection and valacyclovir treatment in schizophrenia: Results from the VISTA study |
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