Epidemiology of the oropouche virus is the study of the distribution and determinants of the infection or disease caused by the virus in human and animal populations. Epidemiology can help understand the risk factors, transmission modes, prevalence, incidence, morbidity, mortality, and control measures of the oropouche virus.
The following are some oropouche virus epidemiology features:
Host range: Oropouche virus (OROV) is an arthropod-borne orthobunyavirus that can infect many hosts, including sloths, marsupials, primates, birds, and humans. Humans are accidental hosts that acquire the infection from the bite of infected midges or mosquitoes. OROV causes oropouche fever (OROF), a febrile illness like dengue fever. OROV is the second most prevalent arbovirus in South America after dengue virus.
Transmission modes: OROV can be transmitted by two primary cycles: a sylvatic cycle and an urban cycle. The sylvatic cycle involves the transmission of OROV among wild animals, such as sloths and monkeys, by mosquitoes, such as Aedes serratus and Culex quinquefasciatus. The urban cycle involves the transmission of OROV among humans by midges, such as Culicoides paraensis and Culicoides furens. The urban cycle can be initiated by introducing OROV from the sylvatic cycle by spillover events or human movement.
Morbidity and mortality: The prevalence and fatality rates of OROV infection or disease depend on the host’s immune status, the viral strain, and the availability of treatment. Sudden onset of fever, headache, myalgia, arthralgia, dizziness, photophobia, vomiting, rash, and retro-orbital pain characterizes OROF. The symptoms usually last for 3 to 7 days and resolve spontaneously. However, some cases may have a biphasic course with a recurrence of symptoms after a brief recovery period. OROF is rarely fatal, and no deaths have been reported to date. However, OROF can cause significant economic and social impacts due to absenteeism from work or school.
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Family: Peribunyaviridae
Genus: Orthobunyavirus
Species: Oropouchevirus
Oropouche virus has a spherical structure with an average diameter of approximately 100-120 nanometers. Its genome is comprised of three segments of single-stranded RNA, referred to as small (S), medium (M), and large (L) segments. Each segment encodes specific proteins that are essential for viral replication and infection.
The S segment encodes the nucleocapsid protein (N), encapsulating the viral RNA. The M segment encodes for the precursor polyprotein, which is cleaved into two glycoproteins, Gn and Gc, involved in viral entry and fusion with host cells.
The virus is enveloped, meaning its exterior lipid bilayer is derived from the host cell’s membrane. This envelope contains viral glycoproteins facilitating viral attachment and entry into host cells.
The pathogenesis of OROV infection is poorly understood, but some studies have provided insights into viral replication, dissemination, and host immune response.
OROV infects various cell types, including endothelial cells, fibroblasts, macrophages, and dendritic cells. The virus enters the cells by receptor-mediated endocytosis and uncoats in the endosomes. The viral genome segments are released into the cytoplasm and transcribed by the viral RdRp to produce mRNAs and antigenomes. The mRNAs are translated into viral proteins, while the antigenomes serve as templates for synthesizing new genomic RNAs. The viral RNAs and proteins assemble into nucleocapsids in the cytoplasm and bud from the plasma membrane to form new virions.
OROV spreads from the inoculation site (skin or mucosa) to the regional lymph nodes and the bloodstream, causing viremia. The virus can reach the central nervous system and breach the blood-brain barrier. (CNS), causing inflammation and neuronal damage. In a mouse model of OROV infection, the virus was detected in the brain, spinal cord, cerebellum, and olfactory bulb five days post-infection. The virus also induced apoptosis, microglial activation, and cytokine production in the CNS.
The host immune response to OROV infection involves both innate and adaptive immunity. The innate immune system recognizes OROV through pattern recognition receptors (PRRs) such as RIG-I-like receptors (RLRs) and Toll-like receptors (TLRs). These receptors activate signaling pathways that produce type I interferons (IFNs) and pro-inflammatory cytokines. Type I IFNs bind to their receptor (IFNAR) and induce the expression of interferon-stimulated genes (ISGs) that have antiviral and immunomodulatory functions. Pro-inflammatory cytokines recruit and activate immune cells such as natural killer (NK), macrophages, and T cells.
The adaptive immune response to OROV infection involves both humoral and cellular immunity. The humoral immune response consists of the production of neutralizing antibodies that can prevent viral entry and infection. The cellular immune response involves activating cytotoxic T lymphocytes (CTLs) that can kill infected cells and secrete cytokines that enhance antiviral immunity.
The host defense pathways that control OROV infection and disease have been investigated using knockout mice that lack critical components of these pathways. It was found that mice deficient in MAVS, IRF-3, IRF-7, IFN-β, or IFNAR were more susceptible to OROV infection and had higher viral loads, more severe clinical signs, and higher mortality than wild-type mice. These results indicate that the RLR-MAVS-IRF-type I IFN axis is essential for controlling OROV infection and pathogenesis.
Oropouche fever is an acute febrile disease, like dengue fever, with typical clinical symptoms such as fever, headache, muscle and joint pain, and skin rash, which may develop into meningitis and encephalitis.
The incubation period is typically 4 to 8 days from the infected mosquito’s bite or midge. The most typical symptom, with temperatures reaching 104F, is fever. There have also been instances where individuals had rashes that resembled rubella and showed various symptoms, such as nausea, vomiting, diarrhea, conjunctivitis, epigastric discomfort, and retroorbital pain.
The diagnosis of OROV infection can be made by using various methods, such as:
Virus isolation: This method involves inoculating the patient’s blood or cerebrospinal fluid (CSF) into cell cultures or newborn mice and observing the cytopathic effects or clinical signs of infection. This method is sensitive and specific but requires biosafety level 3 facilities and trained personnel.
Serology: This method involves detecting the presence of specific antibodies against OROV in the patient’s serum or CSF. The most used techniques are enzyme-linked immunosorbent assay (ELISA), hemagglutination inhibition (HI), and neutralization tests. This method is simple and inexpensive, but it may cross-react with other related viruses and requires paired samples to confirm the seroconversion.
Molecular detection: This method involves amplifying and detecting the viral RNA or DNA in the patient’s blood or CSF using polymerase chain reaction (PCR) or other nucleic acid amplification techniques. This method is rapid and accurate but requires specialized equipment and reagents.
The prevention of OROV infection can be done by using various strategies, such as:
Vector control: This strategy reduces the breeding and biting of midges and mosquitoes that transmit OROV. It can be done by removing or modifying their breeding sites, such as stagnant water, organic matter, or tree holes; applying insecticides or larvicides; or using personal protective measures, such as repellents, bed nets, or clothing.
Surveillance and outbreak response: This strategy involves monitoring the occurrence and distribution of OROV cases and vectors; alerting the health authorities and the public; and implementing appropriate measures to contain and control the outbreaks, such as case management, isolation, quarantine, or vaccination.
Vaccine development: This strategy involves developing and testing safe and effective vaccines against OROV that can induce protective immunity in humans. No licensed vaccine for OROV exists, but some candidates are under preclinical or clinical evaluation.
Oropouche Virus – an overview | ScienceDirect Topics
Epidemiology of the oropouche virus is the study of the distribution and determinants of the infection or disease caused by the virus in human and animal populations. Epidemiology can help understand the risk factors, transmission modes, prevalence, incidence, morbidity, mortality, and control measures of the oropouche virus.
The following are some oropouche virus epidemiology features:
Host range: Oropouche virus (OROV) is an arthropod-borne orthobunyavirus that can infect many hosts, including sloths, marsupials, primates, birds, and humans. Humans are accidental hosts that acquire the infection from the bite of infected midges or mosquitoes. OROV causes oropouche fever (OROF), a febrile illness like dengue fever. OROV is the second most prevalent arbovirus in South America after dengue virus.
Transmission modes: OROV can be transmitted by two primary cycles: a sylvatic cycle and an urban cycle. The sylvatic cycle involves the transmission of OROV among wild animals, such as sloths and monkeys, by mosquitoes, such as Aedes serratus and Culex quinquefasciatus. The urban cycle involves the transmission of OROV among humans by midges, such as Culicoides paraensis and Culicoides furens. The urban cycle can be initiated by introducing OROV from the sylvatic cycle by spillover events or human movement.
Morbidity and mortality: The prevalence and fatality rates of OROV infection or disease depend on the host’s immune status, the viral strain, and the availability of treatment. Sudden onset of fever, headache, myalgia, arthralgia, dizziness, photophobia, vomiting, rash, and retro-orbital pain characterizes OROF. The symptoms usually last for 3 to 7 days and resolve spontaneously. However, some cases may have a biphasic course with a recurrence of symptoms after a brief recovery period. OROF is rarely fatal, and no deaths have been reported to date. However, OROF can cause significant economic and social impacts due to absenteeism from work or school.
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Family: Peribunyaviridae
Genus: Orthobunyavirus
Species: Oropouchevirus
Oropouche virus has a spherical structure with an average diameter of approximately 100-120 nanometers. Its genome is comprised of three segments of single-stranded RNA, referred to as small (S), medium (M), and large (L) segments. Each segment encodes specific proteins that are essential for viral replication and infection.
The S segment encodes the nucleocapsid protein (N), encapsulating the viral RNA. The M segment encodes for the precursor polyprotein, which is cleaved into two glycoproteins, Gn and Gc, involved in viral entry and fusion with host cells.
The virus is enveloped, meaning its exterior lipid bilayer is derived from the host cell’s membrane. This envelope contains viral glycoproteins facilitating viral attachment and entry into host cells.
The pathogenesis of OROV infection is poorly understood, but some studies have provided insights into viral replication, dissemination, and host immune response.
OROV infects various cell types, including endothelial cells, fibroblasts, macrophages, and dendritic cells. The virus enters the cells by receptor-mediated endocytosis and uncoats in the endosomes. The viral genome segments are released into the cytoplasm and transcribed by the viral RdRp to produce mRNAs and antigenomes. The mRNAs are translated into viral proteins, while the antigenomes serve as templates for synthesizing new genomic RNAs. The viral RNAs and proteins assemble into nucleocapsids in the cytoplasm and bud from the plasma membrane to form new virions.
OROV spreads from the inoculation site (skin or mucosa) to the regional lymph nodes and the bloodstream, causing viremia. The virus can reach the central nervous system and breach the blood-brain barrier. (CNS), causing inflammation and neuronal damage. In a mouse model of OROV infection, the virus was detected in the brain, spinal cord, cerebellum, and olfactory bulb five days post-infection. The virus also induced apoptosis, microglial activation, and cytokine production in the CNS.
The host immune response to OROV infection involves both innate and adaptive immunity. The innate immune system recognizes OROV through pattern recognition receptors (PRRs) such as RIG-I-like receptors (RLRs) and Toll-like receptors (TLRs). These receptors activate signaling pathways that produce type I interferons (IFNs) and pro-inflammatory cytokines. Type I IFNs bind to their receptor (IFNAR) and induce the expression of interferon-stimulated genes (ISGs) that have antiviral and immunomodulatory functions. Pro-inflammatory cytokines recruit and activate immune cells such as natural killer (NK), macrophages, and T cells.
The adaptive immune response to OROV infection involves both humoral and cellular immunity. The humoral immune response consists of the production of neutralizing antibodies that can prevent viral entry and infection. The cellular immune response involves activating cytotoxic T lymphocytes (CTLs) that can kill infected cells and secrete cytokines that enhance antiviral immunity.
The host defense pathways that control OROV infection and disease have been investigated using knockout mice that lack critical components of these pathways. It was found that mice deficient in MAVS, IRF-3, IRF-7, IFN-β, or IFNAR were more susceptible to OROV infection and had higher viral loads, more severe clinical signs, and higher mortality than wild-type mice. These results indicate that the RLR-MAVS-IRF-type I IFN axis is essential for controlling OROV infection and pathogenesis.
Oropouche fever is an acute febrile disease, like dengue fever, with typical clinical symptoms such as fever, headache, muscle and joint pain, and skin rash, which may develop into meningitis and encephalitis.
The incubation period is typically 4 to 8 days from the infected mosquito’s bite or midge. The most typical symptom, with temperatures reaching 104F, is fever. There have also been instances where individuals had rashes that resembled rubella and showed various symptoms, such as nausea, vomiting, diarrhea, conjunctivitis, epigastric discomfort, and retroorbital pain.
The diagnosis of OROV infection can be made by using various methods, such as:
Virus isolation: This method involves inoculating the patient’s blood or cerebrospinal fluid (CSF) into cell cultures or newborn mice and observing the cytopathic effects or clinical signs of infection. This method is sensitive and specific but requires biosafety level 3 facilities and trained personnel.
Serology: This method involves detecting the presence of specific antibodies against OROV in the patient’s serum or CSF. The most used techniques are enzyme-linked immunosorbent assay (ELISA), hemagglutination inhibition (HI), and neutralization tests. This method is simple and inexpensive, but it may cross-react with other related viruses and requires paired samples to confirm the seroconversion.
Molecular detection: This method involves amplifying and detecting the viral RNA or DNA in the patient’s blood or CSF using polymerase chain reaction (PCR) or other nucleic acid amplification techniques. This method is rapid and accurate but requires specialized equipment and reagents.
The prevention of OROV infection can be done by using various strategies, such as:
Vector control: This strategy reduces the breeding and biting of midges and mosquitoes that transmit OROV. It can be done by removing or modifying their breeding sites, such as stagnant water, organic matter, or tree holes; applying insecticides or larvicides; or using personal protective measures, such as repellents, bed nets, or clothing.
Surveillance and outbreak response: This strategy involves monitoring the occurrence and distribution of OROV cases and vectors; alerting the health authorities and the public; and implementing appropriate measures to contain and control the outbreaks, such as case management, isolation, quarantine, or vaccination.
Vaccine development: This strategy involves developing and testing safe and effective vaccines against OROV that can induce protective immunity in humans. No licensed vaccine for OROV exists, but some candidates are under preclinical or clinical evaluation.
Oropouche Virus – an overview | ScienceDirect Topics
Epidemiology of the oropouche virus is the study of the distribution and determinants of the infection or disease caused by the virus in human and animal populations. Epidemiology can help understand the risk factors, transmission modes, prevalence, incidence, morbidity, mortality, and control measures of the oropouche virus.
The following are some oropouche virus epidemiology features:
Host range: Oropouche virus (OROV) is an arthropod-borne orthobunyavirus that can infect many hosts, including sloths, marsupials, primates, birds, and humans. Humans are accidental hosts that acquire the infection from the bite of infected midges or mosquitoes. OROV causes oropouche fever (OROF), a febrile illness like dengue fever. OROV is the second most prevalent arbovirus in South America after dengue virus.
Transmission modes: OROV can be transmitted by two primary cycles: a sylvatic cycle and an urban cycle. The sylvatic cycle involves the transmission of OROV among wild animals, such as sloths and monkeys, by mosquitoes, such as Aedes serratus and Culex quinquefasciatus. The urban cycle involves the transmission of OROV among humans by midges, such as Culicoides paraensis and Culicoides furens. The urban cycle can be initiated by introducing OROV from the sylvatic cycle by spillover events or human movement.
Morbidity and mortality: The prevalence and fatality rates of OROV infection or disease depend on the host’s immune status, the viral strain, and the availability of treatment. Sudden onset of fever, headache, myalgia, arthralgia, dizziness, photophobia, vomiting, rash, and retro-orbital pain characterizes OROF. The symptoms usually last for 3 to 7 days and resolve spontaneously. However, some cases may have a biphasic course with a recurrence of symptoms after a brief recovery period. OROF is rarely fatal, and no deaths have been reported to date. However, OROF can cause significant economic and social impacts due to absenteeism from work or school.
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Family: Peribunyaviridae
Genus: Orthobunyavirus
Species: Oropouchevirus
Oropouche virus has a spherical structure with an average diameter of approximately 100-120 nanometers. Its genome is comprised of three segments of single-stranded RNA, referred to as small (S), medium (M), and large (L) segments. Each segment encodes specific proteins that are essential for viral replication and infection.
The S segment encodes the nucleocapsid protein (N), encapsulating the viral RNA. The M segment encodes for the precursor polyprotein, which is cleaved into two glycoproteins, Gn and Gc, involved in viral entry and fusion with host cells.
The virus is enveloped, meaning its exterior lipid bilayer is derived from the host cell’s membrane. This envelope contains viral glycoproteins facilitating viral attachment and entry into host cells.
The pathogenesis of OROV infection is poorly understood, but some studies have provided insights into viral replication, dissemination, and host immune response.
OROV infects various cell types, including endothelial cells, fibroblasts, macrophages, and dendritic cells. The virus enters the cells by receptor-mediated endocytosis and uncoats in the endosomes. The viral genome segments are released into the cytoplasm and transcribed by the viral RdRp to produce mRNAs and antigenomes. The mRNAs are translated into viral proteins, while the antigenomes serve as templates for synthesizing new genomic RNAs. The viral RNAs and proteins assemble into nucleocapsids in the cytoplasm and bud from the plasma membrane to form new virions.
OROV spreads from the inoculation site (skin or mucosa) to the regional lymph nodes and the bloodstream, causing viremia. The virus can reach the central nervous system and breach the blood-brain barrier. (CNS), causing inflammation and neuronal damage. In a mouse model of OROV infection, the virus was detected in the brain, spinal cord, cerebellum, and olfactory bulb five days post-infection. The virus also induced apoptosis, microglial activation, and cytokine production in the CNS.
The host immune response to OROV infection involves both innate and adaptive immunity. The innate immune system recognizes OROV through pattern recognition receptors (PRRs) such as RIG-I-like receptors (RLRs) and Toll-like receptors (TLRs). These receptors activate signaling pathways that produce type I interferons (IFNs) and pro-inflammatory cytokines. Type I IFNs bind to their receptor (IFNAR) and induce the expression of interferon-stimulated genes (ISGs) that have antiviral and immunomodulatory functions. Pro-inflammatory cytokines recruit and activate immune cells such as natural killer (NK), macrophages, and T cells.
The adaptive immune response to OROV infection involves both humoral and cellular immunity. The humoral immune response consists of the production of neutralizing antibodies that can prevent viral entry and infection. The cellular immune response involves activating cytotoxic T lymphocytes (CTLs) that can kill infected cells and secrete cytokines that enhance antiviral immunity.
The host defense pathways that control OROV infection and disease have been investigated using knockout mice that lack critical components of these pathways. It was found that mice deficient in MAVS, IRF-3, IRF-7, IFN-β, or IFNAR were more susceptible to OROV infection and had higher viral loads, more severe clinical signs, and higher mortality than wild-type mice. These results indicate that the RLR-MAVS-IRF-type I IFN axis is essential for controlling OROV infection and pathogenesis.
Oropouche fever is an acute febrile disease, like dengue fever, with typical clinical symptoms such as fever, headache, muscle and joint pain, and skin rash, which may develop into meningitis and encephalitis.
The incubation period is typically 4 to 8 days from the infected mosquito’s bite or midge. The most typical symptom, with temperatures reaching 104F, is fever. There have also been instances where individuals had rashes that resembled rubella and showed various symptoms, such as nausea, vomiting, diarrhea, conjunctivitis, epigastric discomfort, and retroorbital pain.
The diagnosis of OROV infection can be made by using various methods, such as:
Virus isolation: This method involves inoculating the patient’s blood or cerebrospinal fluid (CSF) into cell cultures or newborn mice and observing the cytopathic effects or clinical signs of infection. This method is sensitive and specific but requires biosafety level 3 facilities and trained personnel.
Serology: This method involves detecting the presence of specific antibodies against OROV in the patient’s serum or CSF. The most used techniques are enzyme-linked immunosorbent assay (ELISA), hemagglutination inhibition (HI), and neutralization tests. This method is simple and inexpensive, but it may cross-react with other related viruses and requires paired samples to confirm the seroconversion.
Molecular detection: This method involves amplifying and detecting the viral RNA or DNA in the patient’s blood or CSF using polymerase chain reaction (PCR) or other nucleic acid amplification techniques. This method is rapid and accurate but requires specialized equipment and reagents.
The prevention of OROV infection can be done by using various strategies, such as:
Vector control: This strategy reduces the breeding and biting of midges and mosquitoes that transmit OROV. It can be done by removing or modifying their breeding sites, such as stagnant water, organic matter, or tree holes; applying insecticides or larvicides; or using personal protective measures, such as repellents, bed nets, or clothing.
Surveillance and outbreak response: This strategy involves monitoring the occurrence and distribution of OROV cases and vectors; alerting the health authorities and the public; and implementing appropriate measures to contain and control the outbreaks, such as case management, isolation, quarantine, or vaccination.
Vaccine development: This strategy involves developing and testing safe and effective vaccines against OROV that can induce protective immunity in humans. No licensed vaccine for OROV exists, but some candidates are under preclinical or clinical evaluation.
Oropouche Virus – an overview | ScienceDirect Topics
2020-E000398 (who.int)
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