Revised: May 18, 2026
Accepted: June 29, 2026
Published online: September 25, 2026
Processing time: 189 Days and 21.4 Hours
The Junin virus (JUNV) is mainly perpetuated in nature by rodent reservoirs, especially Calomys musculinus, and is transmitted to humans through aerosolization of contaminated rodent excreta. Clinical presentation of Argentine haemo
Core Tip: Junin virus is a rodent-borne arenavirus that causes Argentine haemorrhagic fever (AHF), a serious viral disease endemic to agricultural regions of Argentina. The infection spreads mainly through contact with contaminated rodent urine, saliva, or feces, often via inhalation of aerosolized particles. AHF initially presents with fever, fatigue, muscle pain, and headache, but severe cases may progress to bleeding disorders, neurological complications, and cardiovascular instability. The disease pathogenesis involves immune system disruption, vascular injury, and coagulation abnormalities. Diagnosis depends on laboratory methods such as reverse transcription polymerase chain reaction, serological assays, and viral isolation. Early treatment with immune plasma therapy can significantly reduce mortality. Prevention strategies focus on rodent control, safe agricultural practices, public awareness, and vaccination with the Candid #1 vaccine in endemic areas.
- Citation: Karanam SK, Uppala PK, Kandra NV, Edhi S. Junín virus and Argentine haemorrhagic fever: Virology, pathogenesis, diagnosis, and prevention strategies. World J Virol 2026; 15(3): 121066
- URL: https://www.wjgnet.com/2220-3249/full/v15/i3/121066.htm
- DOI: https://dx.doi.org/10.5501/wjv.121066
Junin virus (JUNV) is a zoonotic pathogen that is the genus Mammarenavirus within the family Arenaviridae. The etiological agent of Argentine haemorrhagic fever (AHF), a severe viral disease that mainly affects rural populations in Argentina is it. The first case of the disease was reported in the early 1950s when outbreaks of hemorrhagic disease were reported among agricultural workers in the Pampas region. Fever, bleeding, and neurologic. These outbreaks were marked by complications and caused the extensive epidemiological investigations[1,2]. In 1958, scientists were able to isolate the causative virus in Junin province, Argentina, leading to it being named JUNV. This finding was one of the first discoveries of a New World arenavirus linked to human disease. Since its discovery, JUNV has emerged as a significant topic of virological research and has contributed significantly to the overall body of knowledge on viral hemorrhagic fevers and zoonotic viral infections[3,4].
JUNV infection is a serious problem in the community in the endemic areas in Argentina. The global geographic distribution of key arenaviruses that cause human disease represented in Figure 1. The timeline of JUNV was outlined in Table 1. The disease is mainly prevalent in agricultural regions where human activities and environment of infected rodent reservoirs overlap[2,5,6]. It is considered that about five million population that resides in endemic areas is under threat of exposure. Human infection normally happens by inhaling aerosol particles polluted with secretions or excreta of infected rodents, especially those living in cultivated farmlands[3,4].
| Year | Event |
| 1953 | First recognized cases of a hemorrhagic illness among agricultural workers in the Pampas region of Argentina |
| 1958 | Isolation and identification of the causative agent, later named Junín virus, in Junín province, Argentina |
| 1960s | Epidemiological studies confirmed rodent reservoirs, particularly Calomys musculinus, as the natural host of the virus |
| 1970s | Development of early diagnostic techniques and experimental treatments, including immune plasma therapy |
| 1980s | Research programs intensified to develop a vaccine for Argentine hemorrhagic fever |
| 1990 | Development of the Candid #1 live attenuated vaccine through collaboration between Argentina and international research institutions |
| 1991 | Large-scale vaccination campaigns initiated in endemic regions of Argentina |
| 2000s | Improvements in molecular diagnostic methods such as RT-PCR for rapid detection of Junín virus infection |
| 2010s | Advances in molecular virology and reverse genetics improved understanding of viral replication and pathogenesis |
| 2020s | Continued surveillance and research on arenaviruses, including genomic studies and development of new antiviral strategies |
Calomys musculinus is a rodent species of the Cricetidae family that is widely distributed in some areas of Argentina, Bolivia and Paraguay, and is the principal natural reservoir of the virus illustrated in Figure 2[3]. The practice of harvesting, storing of grains and activities in the field increase the chances of human contact with infected rodents, thus aiding in the transmission. JUNV is a high-consequence pathogen because it can cause severe disease and outbreaks[2,5,6]. Along with other arenaviruses (including Lassa virus and Machupo virus) it is listed by the Centres for Disease Control and Prevention as a category A priority pathogen due to the potential to cause high mortality as well as its significance in biodefense research[4,7].
The AHF is an acute infectious disease of viral origin, having a broad range of clinical symptoms. The disease usually starts with some nonspecific symptoms, including fever, fatigue, malaise, headache, and muscle pain[2,8]. With the development of the infection, patients can develop gastrointestinal disturbances, haematological abnormalities, haemorrhagic manifestations, and a neurological complication. Severe forms may comprise vascular damage, bleeding disorders, organ dysfunction and can lead to fatal results when left untreated. The untreated AHF has a historic mortality rate of between 15 and 30 percent[4,9].
Figure 3 shows the rodent reservoirs and transmission pathways of arenaviruses associated with viral hemorrhagic fevers. Nevertheless, medical advances in intervention procedures have greatly helped patients[1,8,10]. Immune plasma therapy using plasma of recovered persons has been proven to cause lesser morbidity when administered at an early stage of infection. Also, the development of the live attenuated Candid #1 vaccine has been a significant contributor towards managing the disease in endemic areas, making JUNV one of the few viral haemorrhagic fever agents with a viable vaccine[4,11].
JUNV is an enveloped RNA virus belonging to the family Arenaviridae and genus Mammarenavirus. Members of this family are primarily maintained in rodent reservoirs and may occasionally cause zoonotic infections in humans through exposure to infected rodent excreta or inhalation of contaminated aerosols[2,3,12,13]. Arenaviruses possess a bi-segmented, single-stranded RNA genome with an ambisense coding strategy[1]. They are broadly classified into Old World and New World arenaviruses; Lassa virus belongs to the Old-World group, whereas JUNV and several other South American haemorrhagic fever viruses belong to the New World group[6,13].
The JUNV has been shown to be genetically varied among the circulating strains, which can affect the viral virulence, transmissibility, and host immune responses. Molecular and phylogenetic studies have identified several strains, which have helped in a better understanding of the evolutionary history of the virus[2,12-14]. The most prominent of these is the attenuated Candid #1 strain which has been developed over serial passages and are currently used as a live vaccine in endemic regions[1,10,11]. Genomic studies are ongoing and have continued to offer insight on the diversity of viruses, their evolution and the pathogenicity mechanisms essential in the development of better vaccines, diagnostics and therapeutic measures[14,15].
JUNV is an enveloped virus that is mostly pleomorphic to spherical in shape, with virions ranging from approximately 50-300 nm in diameter[2,3,13]. One of the distinguishing structural features of arenaviruses is the presence of host-derived ribosomes in the viral particles that confer a granular or Sandy appearance to the virions when observed under electron microscopy[2,12,13]. The viral envelope is made from a lipid bi-layer, derived out of the host cell membrane represented in Figure 4. Included inside this envelope are viral glycoprotein spikes, which is very essential in host cell attachment and membrane fusion during infection[12,16-18]. These spikes are made of processed glycoproteins which facilitate the binding of the receptors and the entry of the virus into susceptible host cells The ribonucleoprotein complexes (RNPs) are composed of viral RNA involved with nucleoproteins and viral enzymes required to replicate the virus. Viral infectivity, efficiency of viral replication, and interactions between the host and the virion depend on the structural organization of the virion[15,17].
The JUNV has a single stranded RNA genome that is bi-segmented consisting of a large (L) segment and a small (S) segment and follows a normal ambisense coding strategy of arenaviruses shown in Figure 5[2,12-14]. In the given organization, the genes are inserted in opposite orientation, and division by non-coding intergenic region which regulates the end of transcription and replication of genome. The L segment (7.3 kb) is a coded RNA-dependent RNA polymerase (L protein), which forms part of the viral RNA synthesis process, and the Z protein which is a small regulatory protein involved in the viral assembly and budding process[12-14]. The nucleoprotein that packages viral RNA to form RNPs are encoded by the S segment (approximately 3.5 kb). The glycoprotein precursor (GPC) that is further processed to produce envelope glycoproteins necessary to enter the host cells are also encoded by the S segment (approximately 3.5 kb)[14,16,17]. Stabilizing transcription and replication of the viral RNA are intergenic region secondary structures[13-15].
The JUNV has a genome that expresses four large proteins that regulate replication, assembly and interaction between viruses and their host[2,12-14].
Nucleoprotein: Coats the viral RNA to create RNPs and helps in immune evasion by suppressing the host type-I interferon responses[19].
GPC: A host protein, SKI-1/S1P cleaves the protein into GP1, GP2 and a signal stable peptide. The interaction between GP1 and membrane fusion between GP2 and transferrin receptor-1 is required to bind the receptors[14,16,17].
L protein: This is the viral RNA-dependent RNA polymerase that transcription and replication of the viral genome[2,13,14].
Z protein: A small ring finger protein that controls virion assembly and budding by interactions with host membranes and viral ribonucleoproteins[14,20].
A combination of these proteins helps to regulate the viral life cycle, including cell entry, genome replication, immune modulation and virion assembly. Figure 6 is the schematic representation of life cycle of JUNV[2,12,13,15,17,20].
The causative agent of AHF, JUNV is maintained in nature via a zoonotic transmission cycle between rodent hosts and exposure to the environment. The virus survives mostly in populations of wild rodents that inhabit agricultural ecosystems, especially in the humid pampas of Argentina[5,6]. The human being is incidentally infected when they encounter contaminated environments or rodent excreta that is infected. It is the ecological interaction between rodent reservoirs, environment, and human activity that is critically important to maintain the circulation of viruses and the patterns of their outbreaks. Natural reservoir and transmission dynamics of JUNV are vital in designing an effective prevention and control methods. The risk of human infection greatly depends upon the agricultural activities, the season, and the rodent population density[2].
The main natural reservoir of JUNV is the drylands vesper mouse, Calomys musculinus, a rodent species of the family Cricetidae. The species is commonly found in the agricultural areas of Argentina and in some areas of neighbouring countries like Bolivia and Paraguay. Rodents infected with JUNV normally have persistent and asymptomatic infections, which enable the virus to persist in infecting rodent populations without causing any significant mortality (Figure 7)[2,6]. Infected rodents transmit the virus to soil, vegetation, stored grains, and dust particles in the agricultural environment. Since these rodents survive in the cultivated fields and grain storage facilities, there are high chances of environmental contamination[2,5,6].
Rodent population density is an important determinant of disease incidence. Research has demonstrated that the greater the densities of Calomys musculinus, the greater the numbers of human cases of AHF. Rainfall, crop cycles and food resource availability are some of the environmental factors that affect rodent population dynamics and hence the distribution of viruses[5,6].
The JUNV transmission cycle mainly involves rodents and their surrounding. The virus creates long-term infections in the hosts of the reservoir and infects rodents through close contact, aggressive behavior, and sharing of common habit
Exposure is likely to be caused by activities like crop handling, cleaning grain storage facilities, and working in fields[2,5,6]. The predominant population affected by the Argentine hemorrhagic fever is rural agricultural workers especially males between the ages of 15 and 60 years. The trend portrays working in the environment where rodents are infected. There is also the increased risk to the rural populations living close to grain storage facilities or close to the agricultural fields[2,5,6].
Human infection risk is caused by several factors, such as: Exposure to the job during farming, harvesting, and hand
Even though some of the exposures have been eliminated by the improvements in agricultural mechanization and housing conditions, JUNV is still a significant occupational hazard in endemic regions[2,6].
Viral proliferation may at first be held by early immune responses, but uncontrolled viral transmission and dysregulated inflammatory responses can give rise to severe disease[12,13].
JUNV infects host cells via receptor-mediated infection. The transferrin receptor 1 on the surface of susceptible host cells, specifically macrophages, dendritic cells, and endothelial cells is bound by the viral surface glycoprotein GP1. This process initiates receptor-mediated endocytosis that enables the virus to penetrate the host cell[12,17]. When the virus gets into the cell, it is carried into endosomes. The viral GP2 glycoprotein activates due to the acidic environment in the endosome and facilitates fusion of the viral envelope and the endosomal membrane. This fusion introduces viral RNPs into the cytoplasm. Viral replication is completely in the cytoplasm[13,17]. Viral RNA-dependent RNA polymerase initially synthesizes messenger RNA to result in the synthesis of proteins. Anthigenomic RNA intermediates are then produced which are templates of the production of new genomic RNA[13].
Viral RNA newly synthesized is associated with nucleoproteins to yield RNPs. These complexes react with the viral Z protein that guides viral assembly at the cell membrane. The virions then bud off the plasma membrane, obtaining their lipid envelope and glycoprotein spikes in the process before being released to infect other cells (Figure 6)[17,20].
The host immune response is very important in the determination of the outcome of JUNV infection[12,13]. The nucleoprotein is one of the major viral proteins that are involved in immune evasion by interfering with the host type I inter
Macrophages and dendritic cells that are infected generate inflammatory cytokines that help in the activation of the overall immune system. Consequently, the immune system might not be able to counter the viral replication effectively[10,12,13]. The adaptive immune response entails both the humoral and cellular immune. Antibody neutralization is a significant factor in viral clearance, and this is the reason why the immune plasma therapy works. Moreover, T-cells specific to the virus also play a role in the destruction of the already infected cells and the control of the viral propagation[9,12,13].
The haemorrhagic manifestations of AHF are due to a combination of hematologic abnormalities, endothelial dysfunc
JUNV causes an acute viral disease, AHF, which can be a mild febrile illness, or severe systemic disease with haemorrhagic and neurological complications. In most cases, the clinical course is characterized by several stages, starting with nonspecific symptoms and possibly progressing to severe system involvement in case of no treatment. The incubation period typically lasts between 7-14 days after exposure to rodent excreta with an infected rodent or infected aerosols. The severity of diseases depends on the viral load, the host immune response, and the time of medical intervention. The diagnosis and treatment at an early stage are some of the most important factors that can positively impact clinical outcomes.
Early stage of Argentine hemorrhagic fever is usually non-specific and flu-like, and it can be difficult to diagnose early in the disease[2,4]. The initial symptoms of the patient are usually a moderate or high fever with generalized weakness and fatigue. Other typical symptoms are headache, retro orbital pain, myalgia, and arthralgia. Gastrointestinal symptoms like nausea, anorexia and abdominal pain also may arise.
At this prodromal stage, the patients might develop facial flushing, conjunctival congestion, and mild lymphadenopathy. The results of laboratory tests often show leukopenia and thrombocytopenia that are early signs of the progression of the disease. The viral replication and the dysregulation of the immune system are factors contributing to the systemic symptoms such as profound fatigue, malaise and progressive weakness[2,4,8].
Hemorrhagic manifestations that are the result of thrombocytopenia, vascular injury, and coagulation abnormalities are one of the defining features of AHF[2,4,13]. Clinically, patients can be observed as having petechiae on the skin and mucous membranes, gingival bleeding, epistaxis, as well as bleeding of the gastrointestinal or urinary tract. In extreme situations, extensive vascular bleeding may cause hypotension and circulatory instability[2,4,8]. Another valuable feature of progressive illness is its neurological involvement.
Patients might experience fine shakiness in their hands and tongue, hyperreflexia, irritability, confusion, and ataxia[2,4]. It is thought that these neurological symptoms are caused primarily by metabolic abnormalities, immune-mediated damage and systemic inflammatory reactions instead of the direct destruction of neural tissue[2,4,13]. In uncommon instances, extreme neurological complications, including seizures, encephalopathy or coma can occur. Other patients that have recovered AHF may develop late neurologic syndrome (LNS), which is a delayed complication that may manifest several weeks after the acute illness[2,4,8].
Other systemic observations can be hepatosplenomegaly, proteinuria, mild hepatic dysfunction, bone marrow suppression. These are symptomatic of the pervasive systemic implications of viral infection and immune control malfunction[2,4,8,13].
The introduction of immune plasma therapy, depending on the recovered patients, has contributed to a great enhancement in the clinical outcomes[4,8]. The immune plasma therapy administration in the first 7-8 days of the disease can help to reduce mortality to less than 1%-2% in most cases with the immune plasma therapy administration in the first 7-8 days of the illness. Early diagnosis and prompt treatment is therefore highly essential in survival of the patient. Some of the factors affecting prognosis are when the treatment starts, the severity of haematological abnormalities and the presence of neurological symptoms. Those patients receiving early medical care tend to have a slow recovery process over the convalescent period, however, delayed fatigue, weakness and weight loss may persist to the convalescent period. Overall, the advent of vaccination, early diagnosis and supportive care has greatly enhanced survival rates in endemic regions. Nevertheless, the main health issue among the population due to its potential severity and the fact that the virus is still spreading in rodent reservoirs is the AHF[1,2,4,8].
Accurate and timely diagnosis of AHF caused by JUNV is essential for effective patient management and outbreak control[16,21]. Early clinical symptoms of the disease are often nonspecific and may resemble other febrile illnesses such as dengue, leptospirosis, or influenza. Therefore, laboratory confirmation is necessary to establish a definitive diagnosis. Although serological methods are widely used, they may have certain limitations. Cross-reactivity with antibodies against related arenaviruses can occasionally occur, and early diagnosis may be difficult before detectable antibody responses develop represented in[2,4,13,15,22].
Laboratory diagnosis relies on a combination of molecular detection of viral RNA, serological identification of virus-specific antibodies, and virus isolation in specialized laboratories[2,4,13]. The choice of diagnostic method depends on the stage of infection, availability of laboratory infrastructure, and biosafety considerations. Because JUNV is classified as a biosafety level 4 (BSL-4) pathogen, handling infectious material requires strict containment procedures[2-4].
Routine clinical laboratory findings may also support diagnosis. Patients commonly show leukopenia, thrombocytopenia, prolonged bleeding time, and proteinuria, which are characteristic but nonspecific indicators of Argentine hemorrhagic fever[2,4].
Molecular techniques play a crucial role in the early detection of JUNV infection, particularly during the acute phase when viral RNA is present in the bloodstream[16,21]. The various diagnostic methods with principle, advantages and limitation is represented in Table 2. The most widely used molecular method is reverse transcription polymerase chain reaction (RT-PCR), which amplifies viral RNA sequences from patient samples such as whole blood, serum, or plasma represented in Figure 8[2,4,13].
| Diagnostic method | Principle | Specimen | Optimal timing | Advantages | Limitations | Ref. |
| RT-PCR | Detection and amplification of Junín viral RNA after reverse transcription | Whole blood, serum, plasma, occasionally tissue samples | Early acute phase (first 7-10 days during viremia) | Highly sensitive and specific; rapid confirmation of active infection; widely used in reference laboratories | Requires specialized molecular equipment and trained personnel; contamination risk; limited availability in rural endemic settings | [2,4] |
| Real-time RT-PCR (qRT-PCR) | Quantitative detection of viral RNA using fluorescent probes during amplification | Whole blood, serum, plasma | Early acute phase | Rapid and highly sensitive; allows quantification of viral load and monitoring of disease progression | Expensive instrumentation; requires advanced molecular laboratory infrastructure | [2,4] |
| Virus isolation | Cultivation of infectious virus in susceptible cell cultures (e.g., Vero cells) | Blood, serum, tissue samples | Early stage of infection when viremia is present | Gold standard for confirmation; enables viral characterization, sequencing, and research studies | Requires biosafety level-4 containment; slow and labor-intensive; high biohazard risk; rarely used for routine diagnosis | [2,3,13] |
| IgM ELISA | Detection of virus-specific IgM antibodies generated during the early immune response | Serum or plasma | From end of first week of illness onward | Indicates recent infection; relatively simple, cost-effective, and widely used for screening | Not suitable for very early infection; possible cross-reactivity with other arenaviruses | [2,4,8,9] |
| IgG ELISA | Detection of virus-specific IgG antibodies indicating immune response or past exposure | Serum or plasma | Late acute phase or convalescent stage | Useful for seroepidemiological studies, vaccine evaluation, and confirmation of seroconversion | Cannot diagnose early infection; often requires paired sera samples | [1,2,4,10] |
| Antigen detection assays | Detection of viral proteins using specific monoclonal or polyclonal antibodies | Blood, serum, plasma | Early phase of infection | Faster than serological tests; useful when molecular testing is unavailable | Lower sensitivity compared with PCR; limited commercial availability | [2,4,9] |
| Neutralization test (PRNT) | Measurement of virus-neutralizing antibodies capable of inhibiting viral infectivity | Serum | Convalescent phase | Highly specific; considered reference method for assessing protective immunity and vaccine response | Requires live virus and high-containment laboratory; technically demanding and time-consuming | [1,10,18,22,23] |
| Routine laboratory tests (supportive) | Detection of hematological and biochemical abnormalities associated with infection | Whole blood, urine | Any stage of illness | Supports clinical suspicion (e.g., thrombocytopenia, leukopenia, elevated liver enzymes, proteinuria) | Nonspecific; cannot confirm Junín virus infection | [4,8,9] |
RT-PCR provides high sensitivity and specificity and allows rapid confirmation of infection during the first week of illness when viremia is highest. Real-time RT-PCR has further improved diagnostic accuracy by enabling quantitative detection of viral RNA, allowing clinicians to estimate viral load and monitor disease progression[2,4].
These molecular assays are particularly valuable for early diagnosis because antibody responses may not yet be detectable in the initial stage of infection. However, the use of molecular diagnostics requires specialized laboratory equipment, trained personnel, and strict biosafety procedures to prevent laboratory contamination or accidental exposure[2,4].
In addition to conventional PCR methods, advanced molecular technologies such as next-generation sequencing and multiplex PCR assays are increasingly being explored for rapid identification of arenaviruses and surveillance of viral evolution[2,4,13].
Isolation of the virus is the ultimate technique of confirming JUNV infection and is mainly applicable in research purposes and not in routine diagnosis[2,4,13]. Isolation usually consists of inoculating clinical samples like blood, serum or tissue samples into vulnerable cell cultures and observing viral replication. As JUNV is very pathogenic and can be spread by aerosol, isolations of the virus should be carried out in a laboratory of BSL-4. As BSL-4 facilities are not widely available, routine diagnosis in endemic areas mainly relies on molecular and serological methods[2-4]. For point-of-care testing or primary screening in resource-limited settings, basic biosafety precautions should be followed, including use of gloves, masks, eye protection, safe blood collection, leak-proof sample containers, surface disinfection, careful sharps handling, and proper biomedical waste disposal[2,4]. Samples requiring further processing should be securely packed and referred to designated reference laboratories[3,4].
Since the disease may rapidly develop into severe haemorrhagic and neurological events, the early diagnosis and subse
Convalescent plasma therapy, or immune plasma therapy, is regarded as the standard treatment of AHF in endemic areas[2,4,8]. This treatment entails the injection of plasma that has been collected in persons who have already been conquered by JUNV and thus has a high titer of neutralizing antibodies against JUNV. These antibodies attach themselves to circulating viral particles and aid in the reduction of the viral replication of the infected patients[2,8]. Clinical studies have demonstrated that immune plasma therapy is most effective when administered within the first 7-8 days after the onset of symptoms. Early therapy can greatly decrease viremia and avoid further development into severe disease. Mortality with early intervention can be reduced up to 12 percent which emphasizes the significance of early intervention[4,8]. There has also been research into the exact constituents of immune plasma that provide protection. Purified immunoglobulin fraction experiments have demonstrated that IgG antibodies are critical in this regard of protection against lethal infection. Although antibody fragments like Fab can neutralize the virus in the test tube, they do not provide complete protection in animal models, indicating that other immune responses, such as removal of infected cells, contribute to therapeutic efficacy[8,22,23].
Immune plasma therapy is effective but has several limitations. These involve the fact that screened donors are required, the possibility of transfusion-transmitted infections, and a small percentage of treated patients may develop LNS[2,4,8]. LNS can occur weeks following recovery and is typified by symptoms which include ataxia, tremors and cranial nerve anomalies. Thus, although immune plasma remains the standard treatment for AHF, its clinical use is limited by donor availability, antibody-titre variability, transfusion-related safety concerns, and the risk of late neurological complications in a small proportion of treated patients[4,8].
Clinical support is another critical part of the treatment of the patient with AHF. The purpose of supportive care is to stabilize the patient, control complications, and prevent the development of a severe disease[2,4]. Some of the main points of supportive management are attention to fluid balance, monitoring of vital signs, correction of electrolyte abnormalities, and treatment of secondary infections[2,4]. Patients who have severe thrombocytopenia or bleeding complications might need platelet transfusion or any other blood product. Haematological parameters, liver and neurological status should also be closely monitored to identify complications at an early stage[2,4,8]. Recent preclinical evidence has shown that humanized monoclonal antibodies can provide strong protection against Argentine hemorrhagic fever in guinea pig and non-human primate models, indicating their potential as a safer, standardized, and scalable alternative to immune plasma therapy in future clinical use[22,23]. Ribavirin, a nucleoside analogue that interferes with viral RNA synthesis, has been explored as an alternative or second-line therapeutic option for JUNV infection, particularly in situations where immune plasma therapy is unavailable, unsuitable, or contraindicated[2,8,24].
However, the evidence supporting ribavirin in JUNV infection remains limited and context-dependent; therefore, it should not be considered a replacement for early immune plasma therapy when appropriate plasma is available[2,8].
The control of AHF due to JUNV is dependent on the use of vaccination, rodent control and minimization of human exposure to infected reservoir hosts[1,2,4,6,10]. Since the virus is preserved in rodent populations and introduced in the human body as contaminated environmental materials, the primary focus of the public health interventions should be on both immunization of vulnerable population groups and the reduction of risks of various environmental sources in the human body. Vaccination is one of the preventive measures at our disposal, but it has been found to be the most effective strategy of controlling the disease in Argentina which is endemic. Besides vaccination programs, other measures that help in the prevention of the disease include; rodent population control, better practices in grain storage.
The Candid #1 vaccine is an innovation in the prevention of Argentine hemorrhagic fever[1,4,10]. The vaccine strain was based on the XJ strain of JUNV which was initially isolated in a case of fatal illness and subsequently attenuated through serial passages in laboratory systems[1,11]. The attenuated virus strain was shown to induce protective immunity in experimental animal models, including guinea pigs and rhesus macaques. These experiments demonstrated that vaccinated animals were resistant to fatal JUNV challenge, which illustrated high levels of vaccine induced immune responses[1,25]. Later experiments in humans established that the vaccine was safe and immunogenic. Phase I and phase II trials have shown that the vaccine elicits strong immune responses with few side effects[1,4,10]. Consequently, Candid #1 was allowed to be used in Argentina and has since become the main preventive agent against AHF[1,4,10,11].
Clinical trials have demonstrated the Candid #1 vaccine elicits both humoral and cellular immune responses, which are fundamental in protecting against JUNV infection[1,10,11]. In more than 90 percent of vaccinated persons antibodies against the virus can be detected, but the antibodies are usually of lower concentration than those observed after a natural infection[1,10]. Besides antibody production, JUNV specific cellular immunity is developed, in addition to antibody-mediated immunity, in approximately 99 percent of vaccinated individuals.
Humoral and cellular immune responses work together to give long-term protective immunity to most vaccinated individuals. Follow-up studies have shown that in the long term, vaccination with one dose of Candid #1 can provide a high level of protection against infection. Notably, extensive vaccination efforts have validated the efficacy of the vaccine in the prevention of the occurrence of the disease in the endemic areas[1,4,10]. The vaccine has also shown an excellent safety profile. Serious side effects related to the administration of vaccines are uncommon and most individuals who receive the vaccines develop minor or temporary side effects like low-grade fever or injection site pain[1,4,10].
In the wake of the successful development of the Candid #1 vaccine, Argentina initiated targeted vaccination programs in high-risk areas, especially in agricultural areas where the disease is endemic[1,4,10]. The main target of these programs is the vaccination of people that are at higher risk of exposure such as agricultural workers, rural residents and laboratory personnel handling the virus. Argentina has seen the number of cases of Argentine hemorrhagic fever reducing significantly since the introduction of vaccination campaigns. Millions of people in endemic countries have already been vaccinated, and epidemiological surveys have demonstrated that there are significant decreases in the number of disease cases as well as deaths.
Immunization activities are usually coupled with the general health educations and environmental containment activities[1,4,10,11]. These are the rodent control measures, safe food storage measures, awareness measures to reduce human exposure to rodent-infested environments[2,4,6]. Although vaccination programs have been successful in Argentina, vaccination Candid #1 vaccine is not easily available in non-endemic areas. Surveillance, vaccination status and studies of the next generation vaccines continue to be significant to control the disease on a long-term basis. Despite its public-health value, the impact of Candid #1 vaccination depends on sustained vaccine availability, coverage of high-risk populations, active surveillance, and effective implementation in endemic rural communities[1,2,4,6,10,11].
Even though there is no known evidence that the virus has been deliberately weaponized, there are several biological and epidemiological properties that make it a potential area of concern when it comes to biodefense and global health security. These attributes are that it has a relatively high case-fatality rate in untreated infections, has the ability to infect humans by inhaling contaminated aerosols, and can cause widespread fear and disruption in affected populations. Due to these properties, JUNV is one of the viral haemorrhagic fever agents which require stringent biosafety measures and international surveillance[2-4]. The study of the virus is thus under very controlled laboratory conditions and the public health agencies have in place surveillance programs to detect and respond to potential outbreaks[2-4,6,7].
There is also a need to handle clinical specimens which are suspected to contain JUNV with special care of biosafety measures. Procedures involving live virus propagation, isolation, or advanced experimental work require BSL-4 containment and trained personnel[2-4]. However, initial screening in endemic or resource-limited regions may be performed using safer molecular or serological assays with standard precautions.
Peripheral health facilities should minimize sample manipulation, avoid aerosol-generating procedures, use personal protective equipment, disinfect work surfaces, and transport specimens in properly sealed and labelled containers. These measures support early diagnosis while ensuring that high-risk testing is referred to specialized reference laboratories[3,4].
Whereas JUNV has not been reported as a biological weapon, it has several properties that, in theory, would make it an appropriate biological weapon. Transmission of the virus may occur via aerosolized particles, which can be used in transmitting the virus by inhalation. Epidemics of haemorrhagic fever diseases can create a great deal of public interest and can be a strain on healthcare systems, especially in areas with poor medical infrastructures[2-4,7]. These reasons are why JUNV and other related arenaviruses like Lassa virus, and Machupo virus are classified by the Centres for Disease Control and Prevention as category A priority pathogens. The agents in this group are of the greatest concern to the potential threat of bioterrorism because of their ability to cause severe illness, high mortality, and widespread disruption of society[3,6,7].
Preparedness to arenavirus infection faced worldwide is aimed at enhancing the surveillance of the disease, increasing diagnostic capacity, and the creation of effective countermeasures in the form of vaccines and antiviral treatment[2,4,6,22,23]. The surveillance programs in the endemic areas of Argentina are used to monitor the human cases as well as the rodent reservoir populations to provide early warning about the circulation of the virus[4-6]. Such surveillance systems will provide quick action response to potential outbreaks, and direct vaccination campaigns in high-risk locations. The international cooperation is important in tracking down the new viral haemorrhagic fevers[4,6].
These viruses are kept in rodent reservoirs, and on some occasions infect human beings by being in contact with infected rodent excreta. Such viruses are similar in their ecological and epidemiological properties, including being zoonotic through rodent hosts and having the potential to cause severe systemic disease[2-4,6].
Generally, arenaviruses can be classified as either the new world or old-world groups based on geographic distribution and genetic characteristics[2,3]. The new world arenaviruses, such as Junin, Machupo, Guanarito, and Sabiia viruses, are mostly found in the Americas and are linked to haemorrhagic fevers[3,6,26-28]. On the contrary, diseases in Africa are caused by old world arenaviruses like Lassa virus[2,3,7]. Even though these viruses are similar in terms of genome structure and modes of transmission, they differ in terms of reservoir hosts, geographic distribution, and patterns of human-to-human transmission[2,3,6,7].
The emerging arenaviruses are an issue of concern to the global health due to their zoonotic nature and their ability to cause outbreaks. New infections have the potential to be increased by environmental changes, expansion of agricultural activities, and increased human contact with rodent reservoirs. Constant monitoring enhanced the diagnostic ability and research on vaccine and antiviral drugs is therefore critical in early detection and control of emerging arenavirus diseases (Table 3)[2-7,29-34].
| Feature | Genus group | Geographic region | Associated disease | Genome type | Genome segments | Reservoir host | Primary transmission | Cell receptor used | Pathogenesis pattern | Case fatality rate (untreated) | Human-to-human transmission | Typical outbreak pattern | Vaccine availability | Biosafety level | Ref. |
| Machupo virus | New world | Bolivia | Bolivian Hemorrhagic Fever | Bi-segmented ambisense ssRNA | L (polymerase, Z) and S (NP, GP) | Calomys callosus | Rodent excreta | Transferrin receptor-1 | Immune suppression; vascular leakage | 20%-30% | Rare | Rural agricultural areas | None | BSL-4 | [3,6,7,27,29] |
| Junín virus | New world | Argentina | Argentine Hemorrhagic Fever | Same | Same | Calomys musculinus | Rodent exposure | Transferrin receptor-1 | Similar to Machupo | 15%-30% | Limited | Rural Argentina | Candid #1 vaccine | BSL-4 | [1-4,8,12,13] |
| Lassa virus | Old world | West Africa | Lassa Fever | Same | Same | Mastomys natalensis | Rodent contact + human-to-human | α-Dystroglycan | High viremia; immune suppression | 1%-20% | Common | Endemic seasonal outbreaks | None widely licensed | BSL-4 | [31] |
| Guanarito virus | New world | Venezuela | Venezuelan hemorrhagic fever | Same | Same | Zygodontomys brevicauda | Rodent exposure | Transferrin receptor-1 | Similar to Machupo | 20%-30% | Rare | Rural Venezuela | None | BSL-4 | [6,23,28,32] |
| Sabiá virus | New world | Brazil | Brazilian hemorrhagic fever | Same | Same | Suspected rodent | Rodent exposure | Transferrin receptor-1 | Limited data; similar NW pattern | High (limited data) | Rare | Sporadic cases | None | BSL-4 | [6,23,26,34] |
| Chapare virus | New world | Bolivia | Chapare hemorrhagic fever | Same | Same | Suspected rodent | Rodent + healthcare transmission | Likely transferrin receptor-1 | Hemorrhagic disease; immune dysregulation | High in outbreaks | Confirmed | Small outbreaks (2004, 2019) | None | BSL-4 | [6,23,27,34] |
| Lujo virus | Old world lineage | Zambia/Southern Africa | Lujo Hemorrhagic Fever | Same | Same | Suspected rodent | Rodent + nosocomial spread | Unclear/distinct receptor | Severe systemic inflammation | About 80% (2008 outbreak) | Confirmed | Single major outbreak (2008) | None | BSL-4 | [33] |
| LCMV | Old world | Worldwide | Aseptic meningitis/encephalitis | Same | Same | Mus musculus | Rodent exposure; vertical; transplant | α-Dystroglycan | Immune-mediated CNS inflammation | < 1% in healthy adults | Rare | Sporadic global cases | None | BSL-3 (BSL-4 recommended for high-risk work) | [8] |
Recent scientific advances have greatly enhanced the knowledge on JUNV and its role in AHF. The development of molecular virology, immunology, and biotechnology has also led to the development of better methods of studying viral replication, developing vaccines, and identifying effective therapeutic strategies[2,12,13,16,18]. The latest research instruments have also contributed to the increase in the speed of infection detection and the tracing of the evolution of viruses in the endemic areas[2,4,6,14,15].
The creation of reverse genetics tools has significantly increased the study of JUNV. This technology permits scientists to create infectious virus particles using cloned complementary DNA to study in detail the processes of viral replication, gene functioning, and pathogenicity mechanisms[2,13,14]. The systems assist the researchers to study the effects of viral genes on virulence and host immune response[12-14]. Molecular research has also helped to understand the structure and function of viral proteins, especially the glycoprotein complex that mediates entry into the host cells. Structural studies have demonstrated the interaction between viral glycoproteins and host receptors and the viral attachment and fusion with the host membrane can be blocked by neutralizing antibodies[16-18]. These discoveries can be used to develop specific antiviral therapies and better vaccines[18,22-24].
Despite the progress in the research of arenavirus, various aspects of JUNV biology remain unexplored. The exact mechanisms that the virus use to suppress the host immune responses and interferon signalling should be the subject of further research[12,19,21]. Moreover, host factors that impact the severity of the disease and the duration of immunity after vaccinating or having natural infection remain poorly understood and require more research[1,2,10,12]. The detection of biomarkers to predict and respond to treatment in early disease is also an important research priority[2,4,13].
Environmental alterations and increasing agricultural practices could alter the location of rodent reservoirs in Argentina, although haemorrhagic fever of Argentina is largely confined to endemic regions of Argentina[4-6]. The fact that there is increased global travel also increases the chances of imported cases in non-endemic regions. It is thus vital to continuously monitor the rodent population and viral genetic variants to identify any emerging risks and to prevent possible outbreaks[2-6].
Future research should aim at creating new antiviral medications, monoclonal antibody therapy, and next-generation vaccines[11,22-24]. Earlier and better diagnostic instruments and early treatment measures would greatly lower the severity of the disease[2,4]. Furthermore, enhancing vaccination, improved ecological monitoring of rodent reservoirs, and promotion of international cooperation will be necessary to control JUNV and enhance preparedness to related arenavirus infections[2-6].
JUNV is still considered as one of the most important viral haemorrhagic fever pathogens in South America and it still represents a public health concern in endemic regions of Argentina. Rodent reservoirs are thought to maintain the virus in nature, and it is believed that the virus is transmitted to humans through contact with infected rodent excreta. The AHF can cause the severe systemic disease that is characterized by the presence of abnormal haematology, malfunction of the vascular system, and neurological complications. The Candid #1 live attenuated vaccine and the immune plasma therapy have made a significant contribution to the mortality reduction and improved disease control in the endemic areas. Moreover, the development of molecular diagnostic methods and genomic surveillance has led to the improvement of early detection and monitoring of infections. Despite these advances, important limitations remain, including continued viral circulation in rodent reservoirs, restricted availability of specific antiviral options, logistical and safety concerns related to immune plasma therapy, unequal access to vaccination, and the possible emergence of related arenavirus infections. Further research into viral pathogenesis, vaccine development and antiviral therapeutics is necessary to enhance the global preparedness and enhance strategies aimed at the prevention and management of AHF.
I sincerely acknowledge Maharajah’s College of Pharmacy, Vizianagaram for its continuous support and Cooperation for completing this review.
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