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Hantavirus . Stephanie Bagley Eugene Khandros Nicholas Bevins. History. Hantaviruses are rodent-borne viruses which may be transmitted to humans in aerosolized urine, feces, or saliva, and occasionally by bite.

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Stephanie Bagley

Eugene Khandros

Nicholas Bevins

  • Hantaviruses are rodent-borne viruses which may be transmitted to humans in aerosolized urine, feces, or saliva, and occasionally by bite.
  • Hantaviruses often cause either hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS)
  • Other hantaviruses are not known to be human pathogens.
hantavirus outbreak in the us
Hantavirus Outbreak in the US
  • HPS was first described in the United States in May 1993 during the investigation of a cluster of cases of acute adult respiratory distress in the Four Corners region.
  • HPS was found to be caused by a previously unknown hantavirus, Sin Nombre, detected in deer mice.
  • Sin Nombre caused approximately 200 confirmed cases of HPS during the outbreak, that led to a 50% mortality rate.
hantavirus in the us
Hantavirus in the US
  • Prior to the HPS outbreak, the only known hantaviruses were those that caused HFRS
  • At least three other hantaviruses, New York Virus, Bayou Virus, and Black Creek Canal virus have since been confirmed to cause HPS in the U.S.
hps in south america
HPS in South America
  • The discovery of HPS in North America led to retrospective studies in South America.
  • More than 140 cases of HPS confirmed in Argentina.
  • The Andes hantavirus was discovered in long tailed pygmy rice rats in southern Argentina.
  • Andes Virus is the only known hantavirus to be transmitted person-to-person.
history of hfrs
History of HFRS
  • While HPS has only been identified since 1993, HFRS has a much longer and complex history.
  • HFRS may have been recognized in China as early as 1000 years ago.
  • HFRS described in 1913 Russian records
history of hfrs1
History of HFRS

Outbreaks of HFRS in the 1930’s:

  • Russia (1932)
  • Japanese troops in Manchuria (1934)
  • Sweden (1934)
characterization of hfrs
Characterization of HFRS
  • 1934 -Japanese outbreak led to studies by Japanese physicians
  • 1940- Japanese physicians compiled a clinical and pathological description of what was then called “epidemic hemorrhagic fever.”
  • First to implicate mice in disease transmission.
  • Physicians injected filtrates of tissue from Apodemus agrarius carrying the hantavirus Hantaan into human subjects.
history of hfrs2
History of HFRS
  • 1939-Russian studies also implicated mice in disease transmission.
  • 1961- Moscow outbreak affecting 113 of 186 workers linked to rodent shipment
characterization of hfrs1
Characterization of HFRS

1967-Russian scientists Yankovski and Povalishina provide more insight into disease.

  • Incubation period up to 6 weeks
  • Cycles of virus activity parallel population cycles of field mice
  • Transmission of disease occurred via inhalation of dust contaminated by rodent excretions.
recent hfrs cases
Recent HFRS Cases
  • 1951- outbreak in Korea during the war affected 3,200 soldiers and resulted in a 7-15% mortality rate.
  • Korean hemorrhagic fever (KHF) drew widespread international attention and was reclassified as HFRS in 1983 by the WHO.
  • 1983-Several past outbreaks including KHF, “epidemic hemorrhagic fever” , Russian outbreaks all reclassified as HFRS by the WHO

Family Bunyaviridae

5 genera, 250 species

Genus Human disease

Bunyavirus LaCrosse encephalitis, others

Phlebovirus Rift Valley fever, sandfly fever

Nairovirus Crimean-Congo hemorrhagic fever

Tospovirus Plant virus, no known human disease

HantavirusHemorrhagic fever with renal syndrome

Hantavirus pulmonary syndrome

hantavirus genus
Hantavirus Genus
  • Hantavirus Similarities
    • RNA viruses
    • Lipid membrane
    • Tri-segmented genome
  • Hantavirus Differences
    • Hantavirus transmitted through aerosolized rodent urine, feces and saliva.
    • Others genera transmitted through arthropod vectors.
epidemiology and rodent hosts
Epidemiology and Rodent Hosts
  • Each strain of hantavirus has a specific rodent host
  • Hantavirus species appear to have co-evolved with host rodent species
  • Rodents carrying hantavirus are asymptomatic

Transmission of Hantaviruses

Chronically infected rodent

Horizontal transmission of infection by intraspecific aggressive behavior

Virus also present in throat swab and feces

Virus is present in aerosolized excreta, particularly urine

Secondary aerosols, mucous membrane contact, and skin breaches are also sources of infection

Courtesy of CDC

rodent hosts

Virus Strain

Rodent Host


Apodemus agrarius

Apodemus flavicollis


Rattus norvegicus


Bandicota indicus


Microtus pennsylvanicus

Prospect Hill

Clethrionomys glareolus


Sin Nombre

Peromyscus maniculatus

New York

Peromyscus leucopus


Oryzomys palustris

Black Creek Canal

Sigmodon hispidus

Rodent Hosts




new world hantaviruses

New York

Peromyscus leucopus

Sin Nombre

Peromyscus maniculatus

Prospect Hill

Microtus pennsylvanicus


Sigmodon hispidus

Bloodland Lake

Microtus ochrogaster

Isla Vista

Microtus californicus


Oryzomys palustris

Black Creek Canal

Sigmodon hispidus

El Moro Canyon

Reithrodontomys megalotis

Rio Segundo

Reithrodontomys mexicanus


Zygodontomys brevicauda


Unknown Host

Laguna Negra

Calomys laucha

Caño Delgadito

Sigmodon alstoni


Oligoryzomys fulvescens


Necromys benefactus

Rio Mamore

Oligoryzomys microtis


Unknown Host


Oligoryzomys longicaudatus


Oligoryzomys flavescens


Oligoryzomys chacoensis


Akodon azarae


Oligoryzomys longicaudatus

New World Hantaviruses

Courtesy of CDC


Hantavirus Pulmonary Syndrome

Canada (36)

Countries with reported cases of HPS

(no of cases)

Countries with no reported cases of HPS

United States (335)

Panama (31)



Bolivia (20)

Paraguay (74)

Uruguay (23)

Chile (273)

Argentina (404)


Rodent Hosts in the United States

Deer mouse (Peromyscus maniculatus)

Carrier of Sin Nombre strain, primary agent of HPS in the US. 250-300 cases since discovery.

rodent hosts in the united states
Rodent Hosts in the United States

White-footed Mouse (Peromyscus leucopus)

Carrier of New York strain.

molecular biology of hantavirus
Molecular Biology of Hantavirus
  • Physical Properties
  • Structure
  • Genetics
  • Replication Cycle
  • Pathogenesis
molecular biology of hantavirus1
Molecular Biology of Hantavirus
  • Physical Properties
  • Structure
  • Genetics
  • Replication Cycle
  • Pathogenesis
virion properties
Virion Properties
  • Spherical or oval-shaped.
  • 80-120 nm diameter
  • Unique grid-like surface pattern, with 7-8 nm projections
  • Lipid bilayer envelope
  • Granulofilamentous interior
  • Survive 12 hours at 4C, high salt concentration and non-physiological pH.
  • Survives 1-3 days after drying.
  • Exposure to lipid solvents and nonionic detergents destroys viral envelope
molecular biology of hantavirus2
Molecular Biology of Hantavirus
  • Virion Properties
  • Structure
  • Genetics
  • Replication Cycle
  • Pathogenesis
structural proteins
Structural Proteins

Membrane glycoproteins (G1 and G2)

Polymerase (L)

Nucleocapsid proteins (N)

membrane glycoproteins
Membrane Glycoproteins
  • G1: 64-67kDa
  • G2: 54 kDa, highly conserved
  • Integral membrane proteins
  • G1-G2 heterodimers form 8 nm projections on virion surface
  • Cysteine-rich
  • Contain asparagine-linked sugar groups
  • Important in cell entry and pathogenesis
nucleocapsid protein n
Nucleocapsid Protein (N)
  • 48 kDA
  • Complexes with genomic vRNA in virus, as well as with cRNA after infection, but not with mRNA
  • Necessary for virus replication and packaging
polymerase l
Polymerase (L)
  • 247 kDA
  • RNA-dependent RNA polymerase (RdRp)
  • Complexed with ribonucleocapsids in virion
  • Endonuclease activity to cleave host mRNA
  • Transcriptase activity for making cRNA and mRNA from vRNA
  • Helicase activity to unwind vRNA during transcription
molecular biology of hantavirus3
Molecular Biology of Hantavirus
  • Physical Properties
  • Structure
  • Genetics
  • Replication Cycle
  • Pathogenesis
genomic organization
Genomic Organization
  • Tripartite negative sense genome
  • Small (S) segment, 1.7-2.1kb, codes for N nucleocapsid protein
  • Medium (M) segment, 3.6-3.7kb, codes for G1 and G2 glycoproteins
  • Large (L) segment, 6.5 kb, codes for L polymerase protein
panhandle structure
Panhandle Structure
  • Conserved repeated complementary sequences at 5’ and 3’ ends form panhandle structures
  • Viral polymerase transcribes negative-strand vRNA to mRNA
  • Polymerase acts as a endonuclease and cleaves host mRNAs 7-18 nt from the 5’ cap
  • The capped oligonucleotides act as primers required to initiate transcription
  • After transcription is primed and the first repeat of the terminal sequence is transcribed, polymerase slips and realigns the nascent RNA, then continues transcription
  • Viral polymerase transcribes negative-strand vRNA to sense cRNA
  • cRNA is used as template to make more negative-strand vRNA
  • pppG is used to prime cRNA and vRNA synthesis
  • Same “prime and realign” strategy
molecular biology of hantavirus4
Molecular Biology of Hantavirus
  • Physical Properties
  • Structure
  • Genetics
  • Replication Cycle
  • Pathogenesis









  • Viral G1 and G2 glycoproteins interact with cell surface receptors
  • Pathogenic hantaviruses bind 3 integrins
  • Non-pathogenic hantaviruses bind 1 receptors
entry and uncoating
Entry and Uncoating
  • Virus particles bound to integrin receptors are taken in by receptor mediated endocytosis
  • Newly formed vesicles are acidified
  • Acidic environment changes conformation of G1 and G2
  • Viral and cell membrane fuse
  • Genomic material and polymerase are released into cytoplasm
primary transcription
Primary Transcription
  • Transcription of negative sense vRNA to mRNA
  • Viral polymerase (RdRp) transcribes nucleoprotein-coated vRNA
  • Capped oligonucleotides from cell’s own mRNA are used to prime transcription
  • Follows “prime and realign” model
  • L and S segment mRNA is translated on free ribosomes in cytoplasm
  • M segment mRNA translated on ER-bound ribosomes
  • G1 and G2 peptides produced from M mRNA are cleaved cotranslationally
  • Separate signal sequences for G1 and G2 cause ER attachment and embed the peptides in ER membrane (Signal Hypothesis)
genome replication
Genome Replication
  • vRNA is used as a template by viral polymerase to make sense strand cRNA
  • cRNA is used as a template to make more negative strand vRNA
  • More genetic material means more virions produced
secondary transcription
Secondary Transcription
  • Extra vRNA synthesized during replication is used as template to make mRNA
  • Since more template is present after vRNA is replicated, more mRNA can be transcribed, and more viral proteins can be made
virion assembly
Virion Assembly
  • Membrane-bound G1 and G2 peptides are transported to Golgi and carbohydrates are attached by N-linked glycosylation
  • vRNA complexes with N nucleopcapsid protein, forms looped panhandle structure, and complexes with L polymerase
virion release scenario 1
Virion Release – Scenario 1
  • Nucleocapsid complexes bud into the Golgi membrane with G1 and G2 embedded
  • Virion particle is formed inside the Golgi
  • Virions are transported to cell membrane by vesicles and released by exocytosis, just like in secretion
  • Viruses may prefer different cell surfaces for release
virion release scenario 2
Virion Release – Scenario 2
  • Sin Nombre and Black Creek Canal viruses
  • G1 and G2 embedded into cell membrane through Golgi vesicles
  • Virions bud from cell membrane, not through Golgi
molecular biology of hantavirus5
Molecular Biology of Hantavirus
  • Physical Properties
  • Structure
  • Genetics
  • Replication Cycle
  • Pathogenesis
hantavirus and host cells
Hantavirus and Host Cells
  • Virus replication typically halts host macromolecule synthesis
  • Hantavirus replication does not affect host cell’s natural functions
  • Hantavirus release does not require host cell lysis
  • Hantavirus is able to establish a persistent infection in rodent host cells
  • Heterodimeric receptors composed of α and β subunits
  • Present on endothelial cells, macrophages, and platelets – cells affected by Hantavirus infection
  • Normally involved in regulation of endothelial cell adhesion, platelet aggregation, Ca++ channel activation, and extracellular matrix interactions, including cell migration
3 integrins
  • Required for infection by pathogenic Hantaviruses
  • β1 integrins are used by non-pathogenic strains
  • Attachment of G1/G2 proteins of viroid to integrin initiates endocytosis, but also activates the receptor
  • Variation in virus G1/G2 protein may account for severity of disease
hantavirus infection pathogenesis
Hantavirus Infection Pathogenesis
  • Binding of Hantavirus glycoproteins to β3 integrin causes disruption of vascular integrity
  • Capillaries become more permeable
  • Arteriole vasoconstriction and vasodilation are disrupted
  • Binding to platelet receptors affects clotting and platelet function
immune reaction
Immune Reaction
  • Immune system activated against Hantavirus epitopes
  • Virus epitopes expressed on surface of host cells triggers cytotoxic T-cell attack on host tissues
  • Symptoms are consistent with inflammatory response
laboratory diagnosis of hantavirus
Laboratory Diagnosis of Hantavirus
  • Hantavirus is difficult to culture, so morphological identification is difficult
  • RT-PCR using primers for conserved genome regions allows confirmation of infection
  • PCR product can be sequenced and compared to known viral sequence database for species identification
clinical presentation of hantavirus infection
Clinical Presentation of Hantavirus Infection

Three different clinical manifestations of hantavirus infection caused by different viral strains

Hemorrhagic fever with renal syndrome (HFRS)

  • Found in Europe and Asia

Nephropathia Epidemica (NE)

  • Found in Europe

Hantavirus pulmonary syndrome (HPS)

  • Found in north and south America
  • A group of clinically similar diseases that occur throughout Europe and Asia
  • Includes several diseases that formerly had other names, including Korean hemorrhagic fever, epidemic hemorrhagic fever and nephropathia epidemica
  • ~15% fatality
stages of hemorrhagic fever with renal syndrome hfrs
Stages of Hemorrhagic Fever with Renal Syndrome (HFRS)

1)Incubation (4-40 days)

2)Febrile Phase (3-5 days)

3)Hypotensive Phase (hours to days)

4)Oliguric Phase (3-7 days)


5)Diuretic Phase (2-21 days)

6)Convalescent Phase (2-3 months)

febrile phase
Febrile Phase
  • 3-5 days
  • Characterized by fever, chills
  • Headache, severe myalgia (muscle pain), nausea
  • Blurred vision, photophobia, eye pain caused by movement
  • Flushing of face, V-area of the neck and back
  • Petechiae (small red spots on skin)
  • Abdominal pain and back pain.
  • Thirst, edema, hemoconcentration, postural hypotension
hypotensive phase
Hypotensive phase
  • Hours to days
  • Blood pressure decrease, hypovolemia (decreased blood volume), shock
  • Worsening of bleeding manifestations: petechiae, epistaxis (nosebleed), gastrointestinal and intracranial bleeding
  • Levels of urea and creatinine in blood rise, proteinuria (excessive protein in urine)
  • Leukocytosis, thrombocytopenia (decreased # of platelets)
oliguric phase
Oliguric Phase
  • 3-7 days
  • Marked by decreased urine production due to renal (kidney) dysfunction
  • Hypervolemia (high blood volume) leading to hypertension
  • Blood electrolyte imbalance
  • Continuation of hemorrhagic symptoms
  • Severe complications: cardiac failure pulmonary edema (swelling of lungs), and cerebral bleeding
diuretic phase
Diuretic Phase
  • Several days to several weeks
  • Beginning of recovery
  • 3-6 liters of urine/ day; return to normal renal activity
  • Anorexia, fatigue due to dehydration
convalescent phase
Convalescent Phase
  • 2-3 months
  • Progressive improvement in glomerular filtration, renal blood flow, and urine concentrating ability
clinical testing for hfrs
Clinical Testing for HFRS
  • Thrombocytopenia (low platelet count) is a signifier
  • Urine tests for albuminuria (abnormally high amounts of the plasma protein albumin in the urine)
  • Urine tests for microhematuria (microscopic amounts of blood in the urine)
problems diagnosing hfrs
Problems Diagnosing HFRS
  • Early symptoms resemble influenza
  • More serious symptoms of hypotensive phase have acute onset
nephropathia epidemica ne
Nephropathia Epidemica (NE)
  • Puumala hantavirus strain
  • Common mild form of HFRS in Europe
  • Similar sequence of symptoms as HFRS, but much milder
  • Only 6% of serologically confirmed cases require hospitalization
  • 1993 four corners outbreak
  • Cases found in almost all of the Americas
  • ~50% fatality
stages of hantavirus pulmonary syndrome hps
Stages of Hantavirus Pulmonary Syndrome (HPS)
  • Incubation (4-30 days)
  • Febrile phase
  • Cardiopulmonary phase
  • Diuretic phase
  • Convalescent phase
febrile phase1
Febrile Phase
  • 3-5 days
  • Fever, myalgia, malaise
  • Other symptoms: headache, dizziness, anorexia, nausea, vomiting, and diarrhea.
cardiopulmonary phase
Cardiopulmonary Phase
  • 4-24 hours
  • Presentation and rapid progression of shock and pulmonary edema (4-24h non-productive cough and tachypnea (shortness of breath)
  • Hypovolemia due to progressive leakage of high protein fluid from blood to lung interstitium and alveoli
  • Hypotension and oliguria
  • Thrombocytopenia (often present in febrile phase as well)
  • Death within 24-48 hours due to hypoxia (lack of oxygen) and/or myocardial failure
diuretic phase1
Diuretic Phase
  • Several days to several weeks
  • Beginning of recovery
  • Rapid clearance of pulmonary edema
  • Resolution of fever and shock
  • Anorexia, fatigue due to dehydration
convalescent phase1
Convalescent Phase
  • Up to 2 months
  • Results in chronic decreased small-airway volume and diminished alveolar diffusing capacity
clinical testing for hps
Clinical Testing for HPS
  • Many lab tests and radiographs appear normal
  • Serological tests more effective
  • ELISA IgM capture assay, using either SNV, Laguna Negra, or Andes antigens are used in all countries that have previously detected cases
  • Immunofluorescent test for the presence of antibodies
  • Blood analysis also may find thrombocytopenia with platelet count less than 150,000 mm in 98% of cases
problems diagnosing hps
Problems Diagnosing HPS
  • Symptoms often confused with influenza
  • Common signs of upper respiratory disease such as sore throat, sinusitis, and ear pain not usually present
  • Abdominal pain often misinterpreted as appendicitis
  • Many doctors outside endemic regions fail to recognize or have sufficient testing
treatment of hantavirus infection
Treatment of Hantavirus Infection
  • General care, alleviation of symptoms
  • Ribavirin (HFRS)
  • ECMO (HPS)
general care

General treatment for renal failure




General treatment for pulmonary pathology

Administration of oxygen

General Care
extra corporeal membrane oxygenation
Extra Corporeal Membrane Oxygenation
  • Removes blood from the body and artificially removes CO2 and adds O2
  • Costly
  • Difficult
  • Administered intravenously
  • Shown to be effective against HFRS causing strains
  • Not shown to be effective against HPS causing strains

A policy intended to strike with terror those against whom it is adopted; the employment of methods of intimidation; the fact of terrorizing or condition of being terrorized.

considerations of pathogens for use in bioterrorism
Considerations of Pathogens for Use in Bioterrorism
  • Health effects
  • Epidemiology
  • Cost effectiveness
  • Psychological effects
  • Economic impact
cdc classifications
CDC classifications

Category A

  • Highest priority organisms that can be easily disseminated or transmitted form person to person, results in high mortality rates and have the potential for major public health impact, might cause public panic and social disruption, and require special action for public health preparedness.
cdc classifications1
CDC Classifications

Category A

  • Anthrax (bacillus anthracis)
  • Botulism (clostridium botulinum)
  • Plague (Yersinia pestis)
  • Smallpox (variola major)
  • Tularemia (Francisella tularensis)
  • Viral hemorrhagic fevers
cdc classifications2
CDC Classifications

Category B

  • Second highest priority organisms that are moderately easy to disseminate, results in moderate mortality rates, and require specific enhancements of CDC's diagnostic capacity and enhanced disease surveillance.
cdc classifications3
CDC Classifications

Category B

  • Typhus fever
  • Viral encephalitis
  • Ricin toxin
  • Food and water safety threats
cdc classifications4
CDC Classifications

Category C

  • Third highest priority organisms that include emerging pathogens that could be engineered for mass dissemination in the future because of availability, ease of production and dissemination, and potential for high morbidity and mortality rates and major health impact.
cdc classifications5
CDC Classifications

Category C

  • Nipah Virus
  • Crimean-Congo Hemorrhagic Fever virus
  • Yellow fever
  • Multi-drug resistant TB
  • Influenza
  • Rabies
cdc classifications6
CDC Classifications
  • HFRS causing strains are Category A because of high infectivity and morbidity
  • HPS causing strains are Category C because of low infectivity
considerations of pathogens for use in bioterrorism1
Considerations of Pathogens for Use in Bioterrorism
  • Health effects
  • Epidemiology
  • Cost effectiveness
  • Psychological effects
  • Economic impact
health effects
Health Effects
  • High lethality
  • No or ineffective treatment
health effects1
Hemorrhagic Fever with Renal Syndrome

Medium lethality

Dramatic visual change in patients (psychological)

Some success with antiviral treatments

Hantavirus Pulmonary Syndrome

High Lethality

No effective treatment

Health Effects
considerations of pathogens for use in bioterrorism2
Considerations of Pathogens for Use in Bioterrorism
  • Health effects
  • Epidemiology
  • Cost effectiveness
  • Psychological effects
  • Economic impact
  • Medium incubation time in order to cause secondary infections
  • Rodent vector
  • Spread through aerosol
  • HFRS causing strains known to transmit human to human
  • Suspected human to human transmission of HPS causing strain in Argentina (Andes Virus)
andes virus
Andes Virus
  • 1996 outbreak in rural Argentina
  • Spread to people whose only contact was a car ride
  • Spread to several doctors caring for HPS patients
  • Low rodent population in Argentina at the time (early spring)
  • Virus only infectious for 1-3 days outside of a host because of a weak lipid envelope
  • The number of particles needed to cause a human infection is not known
considerations of pathogens for use in bioterrorism3
Considerations of Pathogens for Use in Bioterrorism
  • Health effects
  • Epidemiology
  • Cost effectiveness
  • Psychological effects
  • Economic impact
cost effectiveness
Cost Effectiveness
  • What resources would be required to successfully disseminate Hantavirus into a large population?
cost effectiveness1
Cost Effectiveness
  • Preparation of virus using cell culture (difficult, need training and equipment)
  • Aerosolization?
  • Contaminated water?
  • Creation of infected rodent population?
considerations of pathogens for use in bioterrorism4
Considerations of Pathogens for Use in Bioterrorism
  • Health effects
  • Epidemiology
  • Cost effectiveness
  • Psychological effects
  • Economic impact
psychological effects
Psychological Effects
  • HFRS causes dramatic visual effects in patients
  • HPS would be especially difficult to diagnose outside of its normal range
  • Media coverage ‘super flu’ ‘hemorrhagic fever’

Mouse Virus in City!

Everyone will Die!

“Nothing to Fear” say Liberal ‘Doctors’

considerations of pathogens for use in bioterrorism5
Considerations of Pathogens for Use in Bioterrorism
  • Health effects
  • Epidemiology
  • Cost effectiveness
  • Psychological effects
  • Economic impact
economic impact
Economic Impact

What effect would an outbreak of hantavirus have on the economy?

  • Treatment
  • Disruption of work
  • Hysteria
  • Even a small outbreak could cause a large disruption
why hantavirus would be a good terrorist weapon
Why Hantavirus Would Be a Good Terrorist Weapon
  • There is no cure for HPS infection
  • Fairly long incubation period between infection and onset of symptoms
  • Difficult diagnosis of HPS
  • High lethality of HPS
why hantavirus would not be a good terrorist weapon
Why Hantavirus Would Not Be a Good Terrorist Weapon
  • Low infectivity of HPS
  • Difficult production
  • Not stable
  • Vaccines
  • Hygiene
  • E. Coli expressed truncated nucleocapsid as an immunogen
  • Naked DNA
  • Recombinant non-pathogenic virus
  • Rodent brain-derived
  • Cell culture derived
  • Inactivated virus
  • Prevent aerosolization of virus from rodent excrement
  • Dampen surfaces with detergent before cleaning
  • General hygiene

“Weapons of mass destruction, including evil chemistry and evil biology, are all matters of great concern, not only to the United States but also to the world community”~ John Ashcroft