Bunyavirus, any virus belonging to the family Bunyaviridae. Bunyaviridae is a family of arthropod-borne or rodent-borne, spherical, enveloped RNA viruses. Bunyaviruses are responsible for a number of febrile diseases in humans and other vertebrates. They have either a rodent host or an arthropod vector and a vertebrate host.

1. Bunya virus
Anup Muni Bajracharya

2. Bunya virus
• Bunyavirus, any virus belonging to the family Bunyaviridae.
• a very large family
• single-strand, enveloped RNA viruses (more than 300 viruses)
• consists of five genera of viruses:
• Orthobunyavirus,
• Phlebovirus,
• Nairovirus,
• Hantavirus, and
• Tospovirus (Tospoviruses infect only plants).
• Most transmitted by arthropods (e.g., ticks, mosquitoes,
and sand flies)
• cause serious human disease, including certain types of viral
hemorrhagic fever.

3. Bunya virus
• The name Bunyavirales derives from Bunyamwera where
the original type species Bunyamwera orthobunyavirus was
first discovered.
• Ellioviricetes is named in honor of late virologist Richard
M. Elliott for his early work on bunyaviruses.
• Bunyamwera is a town in Bundibugyo District, Uganda.

4. Four genera that infect animals
• Genus Orthobunyavirus
• contains a large number of viruses that share common genetic
features and are serologically unrelated to viruses in other
genera of the Bunyaviridae.
• are mosquito-borne, but some are transmitted
by sandflies or midges (Culicoides spp.).
• includes a number of pathogens of domestic animals and
humans, including Akabane and La Crosse viruses and their
relatives.
• Genus Phlebovirus
• contains over 50 viruses, all of which are transmitted by
sandflies or mosquitoes.
• contains important pathogens, including Rift Valley fever virus
and the sandfly fever viruses.

5. • Genus Nairovirus
• contains a large number of viruses, most of which are
tick-borne, including the pathogens Nairobi sheep
disease and Crimean–Congo hemorrhagic fever viruses.
• Genus Hantavirus
• also includes a substantial number of viruses,
• are transmitted by persistently infected reservoir
rodent hosts via urine, feces, and saliva
• In humans, several of these viruses from Asia cause
hemorrhagic fever with renal syndrome, whereas those
from Europe are typically associated with a different
and less severe disease syndrome.
• Some of the hantaviruses from the Americas cause a
severe acute respiratory distress syndrome referred to
as “hantavirus pulmonary syndrome.”

6. Figure -Diagrammatic representation of a bunyavirus virion
(A) Gc, Gn, glycoproteins produced by processing of M RNA polyprotein; L, transcriptase encoded by L RNA; L, M, and S
RNA, large, medium, and small RNA segments; N, nucleoprotein encoded by S RNA.
(B) Hepatocyte of a rat infected with Rift Valley fever virus, showing virions budding in Golgi vesicles.
(C) Thin section of mouse brain infected with California encephalitis virus, showing extracellular virions.
(D) Negatively stained Hantaan virus virions, showing the pattern of spike placement in squares that is characteristic of
all hantaviruses.
(E) Negatively stained Rift Valley fever virus virions, showing the delicate spike fringe. Bars represent 100 nm.

7. Genome of Bunyaviruses
• 11–19 kb
• consists of three segments of negative-sense (or ambisense), single-
stranded RNA, designated large (L), medium (M), and small (S), differ in
size
• the L RNA segment (6.3 to 12 kb), encodes a single large protein (L),
the RNA-dependent RNA polymerase.
• the M RNA segment (3.5 to 6 kb), encodes a polyprotein that is processed
to form two glycoproteins (Gn and Gc) and, in some cases, a nonstructural
protein (NSm).
• the S RNA segment from 1 to 2.2 kb, encodes the nucleoprotein (N) and,
for members of the Orthobunyavirus and Phlebovirus genera, a
nonstructural (NSs) protein.

8. Virus Replication
• Viral entry -by receptor-mediated endocytosis; all
subsequent steps take place in the cytoplasm.
• Cell receptors are not described for many bunyaviruses.
• Exception -in hantaviruses, cell receptors include
αβ integrins and other cell receptor proteins such as
gC1qR/p32, which is expressed on endothelial
cells, dendritic cells, lymphocytes, and platelets.
• Because the genome of the single-stranded, negative-
sense RNA ----viruses cannot be translated directly, the
first step after penetration of the host cell and uncoating
is the activation of the virion RNA
polymerase (transcriptase) and its transcription of viral
mRNAs from each of the three virion RNAs.

9. • The RNA polymerase also has endonuclease activity,
cleaving 5′-methylated caps from host mRNAs and adding
these to viral mRNAs to prime transcription (so-called cap
snatching).
• After primary viral mRNA transcription and translation,
replication of the virion RNA occurs and a second round of
transcription begins, with preferential amplification of the
genes that encode structural proteins necessary for virion
synthesis.
• Virions mature by budding through intracytoplasmic
vesicles associated with the Golgi complex and are released
by the transport of vesicles through the cytoplasm and
subsequent exocytosis from the apical and/or basolateral
plasma membranes
Virus Replication

10. Life Cycle

11. Pathogenesis
• Except for members of the
genus Hantavirus, bunyaviruses replicate
in arthropods.
• The gut of the vector is infected initially,
and after a few days or weeks the virus
appears in the saliva; the arthropod then
remains infective for life but is not ill.
• When the vector takes a blood meal, the
infective saliva enters the small capillaries
or lymphatics of the human or other
vertebrate host.
• The primary site of replication in humans
is not known; it may be the vascular
endothelium, the skin, or the regional
lymph nodes. An incubation period of a
few days ensues, after which the
vertebrate host develops viremia.
• Fever accompanies viremia, which seeds
the liver in Rift Valley fever and Crimean-
Congo hemorrhagic fever. Encephalitis,
retinitis, and renal involvement usually
appear later in infection (after antibody
formation).

12. Laboratory Diagnosis Bunyavirus Infections
• by isolating the virus,
• detecting RNA by RT-PCR, or
• by showing a fourfold or greater rise in antibody titer between acute- and
convalescent-phase sera.
• The virus can be isolated from blood (or from brain, liver, and other organs
postmortem) during the viremic phase, but not usually after the third day of fever.
• Virus Isolation - intracranial inoculation of suckling mice is thought to be the most
sensitive system available for virus isolation. However, several sensitive cell culture
systems are available such as vero. LLC-MC2 and mosquito cells. Once isolated the
virus can be types by neutralizing tests.
• Rapid Diagnosis - antigen detection systems and the detection of specific IgM
antibodies are becoming available as means of rapid diagnosis.
• Serology - a wide variety of serological techniques are available such as HI, CFT,
IFA, neutralization tests and ELISAs.

13. Prevention
• depends on the reservoir, amplifying hosts
and how the viruses are transmitted, i.e. the
vector, whether ticks or mosquitoes and which
animals are involved.
• general hygiene
• limiting contact with vector saliva, urine,
feces, or bedding.
• No licensed vaccine for bunyaviruses.

14. References
• https://www.sciencedirect.com/topics/neuroscience/b
unyaviridae
• https://www.ncbi.nlm.nih.gov/books/NBK8004/
• https://viralzone.expasy.org/6776
• https://www.britannica.com/science/bunyavirus
• Textbook of Microbiology and Immunology- S Parija
• The short textbook of Medical Microbiology-Gupte