Abstract: A historical representative of the Poxviridae family of viruses, monkeypox is

notorious for its effects on both human and animal populations. It is a disease that spreads from rats,
squirrels, and monkeys to people by direct contact with contaminated body fluids. The illness presents
with symptoms including fever, headaches, and characteristic skin lesions and has a risk of serious
consequences like pneumonia and sepsis. Although there isn't a permanent cure, supportive care can
help manage symptoms, and the smallpox vaccination has some efficacy in preventing infection. The
virus originally appeared in the 1970s and became well-known following a significant epidemic in
the US in the early 2000s. The disease's epidemiology is found across Central and West Africa, and
occasional outbreaks in non-endemic areas are brought on by international travel and commerce.
Comprehending the architecture and pathogenicity of the virus, particularly its cytoplasmic
replication and host immune evasion tactics, offers a valuable understanding of its processes of
infection. Human-to-human contact, environmental pollution, and zoonotic proliferation are the
modes of transmission; recent research has even raised the possibility of transmission between people
and dogs. Preventive approaches center on sanitation, isolating sick persons, and immunization tactics
despite difficulties with diagnosis and containment. While currently being developed mainly for
smallpox, existing vaccinations provide some protection against monkeypox, such as JYNNEOS, and
efforts are being made to improve their availability and effectiveness. Additional investigation into
the biology, epidemiology, and immunology of monkeypox is essential for creating efficient control
and treatment plans, since the disease continues to be a worldwide health problem.

Keywords: Monkeypox, Poxviridae, Virus.

INTRODUCTION

Throughout human history, there have been several viral outbreaks that have had a major
effect on society and world health. The viruses that cause epidemics include the virus that causes
smallpox, influenza, severe acute respiratory syndrome (SARS), HIV-1, severe acute respiratory
syndrome coronavirus-2 (SARS-CoV-2), Ebola and the virus that causes monkeypox (Berche, 2022).
Monkeypox from the Poxviridae family, is a virus with double-stranded DNA that causes the
uncommon viral illness. Humans become infected by way of animals such as rats, squirrels, and
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monkeys. Humans can contract the virus by coming into intimate contact with body fluids like mucus,
saliva, or skin lesions that are carriers of the virus. Symptoms of the sickness include fever, headaches,
muscular aches, and a rash that begins as little pimples and develops into raised lumps that are fluid-
filled (Harris, 2022). Although they can appear anywhere on the body, monkeypox-related lumps are
typically detected on the hands, feet, and face.

In severe situations, the infection may result in potentially lethal consequences including
sepsis and pneumonia. Although there isn't a particular therapy for monkeypox at the moment,
supportive care can assist manage the symptoms using drugs that lower temperature and discomfort.
Although it is not always successful, there may be some protection against monkeypox from the
smallpox vaccination. It is crucial to avoid contact with afflicted animals and to follow basic
preventive measures to prevent monkeypox include frequent hand washing and avoiding close contact
with sick individuals (Huang et al., 2022). Although there isn't a permanent treatment for monkeypox,
supportive care can help manage its symptoms (Durski, 2018).

In 1970, a 9-month-old infant in the Democratic Republic of the Congo became ill with
monkeypox for the first time. After an epidemic in the United States in 2003–2004, the virus became
well known (Reed et al., 2004). The clinical signs and symptoms of monkeypox are comparable to
those of smallpox. But monkeypox usually has a lower death rate. In the 1970s, when smallpox was
eradicated, the incidence of the virus surged as smallpox vaccination campaigns were discontinued,
drawing attention to monkeypox from all over the world. Despite the fact that macaque monkeys are
not the true carriers of the virus, the name of the virus comes from its first detection in these primates
(Likos et al., 2005; McCollum & Damon, 2014). With sporadic occurrences documented in various
nations, especially in the Western Hemisphere, monkeypox is currently a serious issue. It mostly
spreads through human-to-human contact, either by skin sore contact or inhalation of droplets from
infected patients (De Baetselier et al., 2022). Given the global occurrence. In order to reduce the
morbidity and death rate in the future, it is critical to look into potential treatment options and the
long-term impacts of the virus, given the continued incidence of cases of monkeypox globally (De
Baetselier et al., 2022; Luna et al., 2022).

In this review, the researcher emphasizes the important details and information about
Monkeypox’s extensive history, viral structure, pathogenesis, pathophysiology, epidemiology,
treatment, and future perspectives.

THE HISTORICAL THREADS OF MPXV

One of the numerous zoonotic viruses that are members of the Poxviridae family's
Orthopoxvirus genus is monkeypox; it is further classified into two subfamilies: Chordopoxvirinae
and Entomopoxvirinae. Vertebrates are known to be infected by the subfamily Chordopoxvirinae,
further subdivided into eighteen genera, one of which is Orthopoxvirus (OPXV), to which the
Monkeypox Virus (MPXV) belongs (Likos et al., 2005; McCollum & Damon, 2014). In 1958, MPXV
was initially identified after an epidemic among monkeys at a Danish laboratory (Von Magnus et al.,
1959). The first recorded human case of MPXV was in 1970 when a 9-month-old infant became
infected in the Democratic Republic of the Congo wherein 1968, two years after smallpox had been
declared eliminated in that region (Ladnyj et al., 1972; Reed et al., 2004).

While cases of MPXV are primarily found in the Congo Basin, other Central and West African
countries have also reported cases of monkeypox in humans and animals (Jezek et al., 1988). Thus,
after diseased African animals were transported from Ghana, MPXV was transferred to native
American prairie dogs, which caused the initial outbreak of MPXV outside of Africa. As a result, the
 3

illness spread to five states, and 47 human cases were recorded (Zhang et al., 2022). Following an
outbreak in the United States and international attention after smallpox was eradicated, the virus
received significant notoriety in 2003–2004 as its prevalence rose and smallpox vaccination
campaigns were discontinued (McCollum & Damon, 2014).

VIRAL ARCHITECTURE OF MPXV

Morphology and Genome of MPXV

The morphology of the monkeypox virus is irregular and envelope-shaped, with extra bodies
along the edges and a dumbbell-shaped center. Unlike other DNA viruses, which tend to replicate in
the nucleus, poxviruses do it in the cytoplasm of cells (Davison & Moss, 1989; Upton et al., 2003),
since poxvirus factories are cytoplasmic structures that replicate the DNA of the virus from a single
infecting particle (Kieser et al., 2020). The creation of cavities that include both the host translation
machinery and viral mRNA is a characteristic of the larger, more diverse viral factories that result
from replication (Katsafanas et al., 2007). Rather than depending on cellular proteins, poxviruses
employ a significant amount of their own encoded proteins during reproduction (Baldick, 1993).
Genes essential for the transcription and assembly of the virus within cells are located in the middle
region of the poxvirus genome. Meanwhile, the way the virus and its host interact are mediated by
the terminal genes in the genome (Upton et al., 2003; Yang et al., 2011). Of the 150 genes, 90 are
found in the Chordopoxvirus subfamily and 49 are found in every Poxviridae family member that has
been sequenced. The middle region of the genome contains the bulk of conserved genes. Poxviruses
like monkeypox have difficulty effectively evading host defenses and proliferating quickly due to
their size (Upton et al., 2000).

Pathogenesis of MPVX
The intimate contact between humans or animals is the first step in the transmission of the
monkeypox virus, which is the source of its pathogenicity and pathophysiology. Via the respiratory
or oropharyngeal mucosa of the patient, smallpox and monkeypox can spread. The virus replicates in
the respiratory and oropharyngeal mucosa after entering through the injection site. Primary viremia
is caused by viruses that spread to nearby lymph nodes. However, in secondary viremia, these viruses
infiltrate lymph nodes and organs through blood circulation (Moore et al., 2023) (Figure 1).

Figure 1. The pathogenesis of MPXV (Saijo et al., 2009). CC BY-NC-SA 4.0 DEED.
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This procedure reflects the seven, fourteen, or twenty-one-day incubation period. This virus
is a multiorgan system invasion (Figure 2). The attachment of monkeypox virion is most likely
mediated by extracellular matrix elements, target cell surface glycosaminoglycans that are found
within cells, and external virion proteins. When xenoviruses fuse directly with the plasma membrane
at neutral pH or enter through a low-pH endosomal pathway, viral cores are discharged into the
cytoplasm of host cells. To merge with the cell, mature intracellular virions and enveloped external
virions need 12 non-glycosylated viral membrane proteins combined into a complex (Moss, 2016).
Following entrance, the multi-subunit DNA-dependent RNA polymerase expressed by a virus on host
ribosomes translates the early, intermediate, and late proteins. This process initiates viral
transcription. Poxvirus DNA synthesis takes place in cytoplasmic structures called "factories," which
progressively change from crescent-shaped structures where virion assembly occurs to endoplasmic
reticulum membrane-covered, dense structures containing DNA (Davies et al., 2017). While most
mature virions remain inside the cell, others are carried by microtubules and enclosed in two
membranes produced by the Golgi apparatus or the Endoplasmic reticulum (intracellular mature
virions). These virions have two possible fates: they may leave the cell through the fusion of the
cytoplasmic membrane, or they can start actin polymerization, which forces the actin-tailed particles
in the direction of a nearby cell (Smith et al., 2002).

Figure 2. Involvement of Monkeypox Virus in the multiorgan system (Reynolds et al., 2017. CC
BY-NC-SA 4.0 DEED.

Intracellular Structure of MPVX

Poxviruses have developed a set of virulence genes, which generate chemicals that can control
the host's immune response, to evade discovery. Depending on where they work, these proteins might
be classified as extracellular or intracellular. Intracellular proteins include virostealth proteins, which
obscure immune recognition signals such as CD4 and Major Histocompatibility Complex 1 (MHC1),
and virotransducer proteins, which impair the cell's reaction to the infection (Liszewski et al., 2006).
A viromimic protein is the sole class of extracellular protein. Viromimic proteins may be divided into
two groups: virokines, which mimetic growth factors, chemokines, and host cytokines to promote
viral reproduction and dissemination, and viroreceptors, which bind to host cytokines and chemokines
to interfere and disrupt their activities (Chen et al., 2005). In addition, extracellular enveloped virions
 5

and Mature virions (MVs) are the two types of poxviruses (EVs). Whereas EVs have an extra outer
membrane and aid in the virus's internal transmission within the host, MVs only have one membrane
and are in charge of adhering to host cells (Tolonen et al., 2001). Hence, the virion is created using
crescent-shaped structures formed when endoplasmic reticulum membranes are broken down later in
the replication process by a mix of membrane-forming proteins and viral gene products. To create
immature virions, late viral gene products, and membrane assembly proteins work together to tear
down the endoplasmic reticulum membrane and generate crescent structures (Katsafanas et al., 2007;
Kieser et al., 2020).

BIOLOGICAL MECHANISM OF MPXV

Pathophysiology and Infection of MPXV

Data from human modeling studies and outbreak investigations have enhanced our
understanding of the pathophysiology of human monkeypox infection, and the outcomes of challenge
studies involving prairie dogs and other primates (Grant et al., 2020). The majority of people
experience the disease's clinical symptoms after the incubation phase, which lasts between 5 and 21
days (usually 7 to 14 days). A strong local innate immune response that develops over hours to days
in response to the injection of the MPXV can enter the lungs, upper respiratory tract mucosa, soft
tissues, or skin usually resulting in the fibroblasts, polymorphonuclear leukocytes, and macrophages
recruitment. (Davies et al., 2017). The virus then spreads to the local lymph nodes through the
lymphatic system, following an initial viremic phase in which the tonsillar and splenic tissues are
seeded (Grant et al., 2020). The viscera, which include the testicles, liver, intestines, kidneys, ovaries,
and/or brain, and the integument, seed after a secondary viremic phase. Corneal scarring may occur
as a result of autoinoculation following contact with infectious skin lesions, conjunctival involvement,
or involvement of the eyelids (Nalca et al., 2010). More skin lesions, a greater chance of involvement
of the gastrointestinal tract (small intestine, colon, stomach, pancreas, peritoneal membrane), a
prolonged disease period, more severe symptoms, and a plasma viral load that is ten times higher than
clade II are associated with infection with clade I, formerly referred to as the clade from Central
Africa (formerly known as the West African clade) (Saijo et al., 2009).

Apart from a more severe clinical course and the lack of lymphadenopathy in smallpox, the
histopathologic and clinical aspects of human monkeypox infection are nearly identical to those of
smallpox. Moreover, aerosols are typically used to spread smallpox, but this has not been proven to
work for monkeypox in natural environments (Nalca et al., 2010). Animal bites or scratches can
transfer the virus into the circulation, shortening the incubation time and perhaps preventing
prodromal symptoms (Chen et al., 2005). Many virulence genes that are absent from clade II have
been identified in Clade I; the most significant of these genes seems to be the monkeypox inhibitor
of complement enzymes (MOPICE) gene, which is comparable to the smallpox inhibitor of
complement enzymes (SPICE) gene found in the Variola virus (Chen et al., 2005). It has been
demonstrated that the MOPICE gene encodes a protein that obstructs the host complement cascade's
first stages. Other significant virulence factors found in Clade I include those that encourage cellular
death. Additionally, there is proof that clade I infections cause earlier viremia and more widespread
illness (Hutson et al., 2015).

Mode of Transmission of MPXV

Studies indicate that there are three potential routes of MPXV transmission: from animals to
humans, from humans to humans, and from the contaminated environment to humans, even if the
precise manner of transmission is yet unknown (WHO, 2022).
 6

Zoonotic, or animal-to-human, transmission happens when an infected animal comes into

direct contact with another animal or when an infected animal is handled in any way, such as when
hunting, skinning, trapping, cooking, or playing with carcasses. It can also happen when an animal is
vaccinated from an infectious animal through mucocutaneous lesions, especially when the skin barrier
is compromised from scratches, bites, or other trauma. Transmission may also occur by the ingestion
of undercooked meat from infected nonhuman primates or animals, including tree squirrels,
antelopes, gazelles, rabbits, dormice, porcupines, and Gambian giant squirrels (Fowotade et al.,
2018).

Figure #. The life cycle of MPXV (Petersen et al., 2022). CC BY-NC-SA 4.0 DEED.

Human-to-human transmission can happen when an infected person comes into direct contact
with their skin, mucous membranes, or mucocutaneous lesions. This can happen through oral or
respiratory secretions; face-to-face, skin-to-skin, mouth-to-mouth, or mouth-to-skin contact, and
droplets that need to be in close proximity for an extended period of time (Kannan et al., 2022).
Caregivers and family members are in danger of infection from prolonged contact. It is thought that
the respiratory tract, mucosal surfaces, or damaged skin are the entry points for the virus into the
body. There is evidence linking nosocomial transmission to the MPXV (Petersen et al., 2019). The
current outbreak's high incidence prompts worries about potential sexual transmission. In fact,
samples of feces, urine, sperm, saliva, and rectal swabs from infected patients had significant virus
loads. Research done in Nigeria and Spain has revealed that concurrently there is main zoonotic and
 7

secondary human-to-human transmission. A different Spanish investigation demonstrates that

monkeypox is an emerging infectious disease that is both locally transmitted and community-acquired
(Orviz et al., 2022).

Direct contact with objects (such as sheets, clothes, or towels) contaminated by human fluids,
lesion fluid, crust, or scab by an infected individual may serve as a transmission channel. OPXVs
have a high degree of environmental stability and are generally more resilient to environmental stress
(Orviz et al., 2022). Depending on the parameters of the room, the surrogate pox virus can live for up
to 56 days in the environment and on different surfaces (Kannan et al., 2022). On the other hand,
information about environmental transmission is currently scarce. As of right now, there is no
information available on MPXV presence in wastewater (Petersen et al., 2019).

A recent article in the Lancet provides strong proof of MPXV transfer from humans to dogs.
The two Paris, France-based household members who were infected with MPX were frequently in
close contact and even shared a bed with the Italian greyhound, who otherwise seemed to be in good
condition (Seang et al., 2022).

IMMUNOLOGY AND EPIDEMIOLOGY OF MPXV

Epidemiology
There is proof that people have been infected by the neglected tropical disease known as the
monkeypox virus (MPXV), which is present in several parts of sub-Saharan Africa. Many confirmed
instances of human monkeypox were recorded in Nigeria in the years that followed, with 10 cases
occurring between 1971 and 1978. The number of human cases of monkeypox documented within
the last three decades has increased (Sabeena, 2023).

In 2017, Nigeria saw the biggest-ever epidemic of the clade II West African variant of
monkeypox. 38 of the 47 cases of monkeypox that were recorded in West and Central Africa between
1970 and 1979 were primarily found in isolated and rural regions of the Democratic Republic of the
Congo. Six instances of monkeypox in uninfected people suddenly appeared in Sierra Leone, Liberia,
and Nigeria between 1970 and 1971; these countries had previously had no recorded occurrences of
smallpox (De Baetselier et al., 2022).

It's interesting to note that outbreaks of monkeypox have been reported in areas where the
illness had not previously been reported. It is not uncommon for MPXV to be found outside of its
endemic locations. A number of outbreaks have been documented in non-endemic regions, such as
the United States in 2003 and Singapore, the United Kingdom, Israel, and Israel in 2017 (Sabeena,
2023). Travelers returning from endemic areas or nosocomial exposure—such as coming into touch
with infected rodents—have been primarily blamed for these outbreaks. The extent and quick spread
of the current MPX pandemic, however, set it apart from other outbreaks in terms of scale. At least
88 countries or territories had reported human-to-human viral transmission by August 5, 2022, and
the number is still rising (De Baetselier et al., 2022; Luna et al., 2022) A possible pandemic has raised
concerns due to the abrupt increase of MPXV cases in nations where it is not normally present.
Because MPXV may spread by droplets or intimate contact with an infected individual, diagnosing
and treating the virus can be difficult. WH declared a Public Health Emergency of International
Concern as a result (WHO, 2020).

Prevention
The following actions can lower your risk of getting monkeypox, according to the Centers for
Disease Control and Prevention (CDC): use an alcohol-based hand sanitizer and wash your hands
 8

frequently before touching your face or eating, and avoid being around someone who has skin-to-skin
interaction with an individual who has rashes similar to monkeypox. (Huang et al., 2022).

To stop the spread of MPXV infection in the community, isolation of patients with mild,
uncomplicated MPX illness, whether proven or suspected is advised for the duration of the infectious
period, provided that a home assessment finds that in the home setting, infection prevention control
(IPC) requirements are satisfied. With the patient's informed permission and the caregiver's and
household members' approval, isolation may need to be set up at a medical institution or other
approved setting if appropriate isolation and IPC measures cannot be ensured at home (WHO, 2020).

The only methods that can effectively prevent monkeypox are infection control measures such
active contact tracing, isolation and quarantine of sick animals, surveillance, enhanced nursing, early
case-finding, sufficient facilities and staffing, and self-monitoring by contacts. In addition to these
precautions, immunizing high-risk contacts with primary preventive vaccination (PPV) and
postexposure preventive vaccination (PEPV) may be beneficial. No matter how many vaccines are
available, mass immunization is neither necessary nor advised to prevent monkeypox,
notwithstanding the results of the current risk and benefit analyses (De Baetselier et al., 2022).

Table 1. For individuals with monkeypox, early supportive treatment and surveillance (WHO, 2022).

Confirmed patients Sever/critical condition MPXV with other MPXV in pregnant

patient disease conditions women
• For fever, an • Antivirals • All HIV- • Pregnant
antipyretic (cidofovir, positive women with
(paracetamol) brincidofivir, patients should mild instances
• Painkillers tecovirimat), if continue of monkeypox
(such as necessary receiving do not require
opioids, • Empiric antibiotic antiretroviral emergency
morphine, treatment for medication in care.
paracetamol, consequences addition to • Watching for
ibuprofen, and such as sepsis, antivirals the
lidocaine gel) proctitis, (tecovirimat, development
• Loratadine, an encephalitis, cidofovir, of a disease
antihistamine, necrotizing soft brincidofovir), • In a medical
for itching tissue infection, opportunistic setting, severe
• Antiemetics pyomyositis, infection cases require
for nausea and conjunctivitis, prophylaxis optimal
vomiting, such and pneumonia (PPV, PEPV), supportive
as (flucloxacillin, and other care.
promethazine cefalexin, related • One crucial
and amoxicillin- treatments. component of
ondansetron clavulanic acid, • Starting supportive
• Omeprazole, a clindamycin, antiretroviral care is patient
PPI, for trimethoprim- medication counseling.
dyspepsia sulfamethoxazole, (ART) for
• ORS for doxycycline). those who have
dehydration • Burn-like skin just received
and diarrhea exfoliation an HIV
• Diazepam treatment diagnosis
(BDZs) with • For severe • The
psychotherapy cervical recommended
course of
 9

to treat adenopathy, treatment for

agitation and steroids people with
anxiety • For rectal both HIV
• If necessary, a discomfort, oral coinfection and
nutritional and topical monkeypox is
supplement analgesia tecovirimat.
(ibuprofen, • Because of the
lidocaine gel, potential for
paracetamol, and nephrotoxicity,
opioids) patients with
• Supportive blood
treatment, such as creatinine
oral laxatives for levels greater
rectal pain with than 1.5 mg/dL
tenesmus and should not use
rectal cidofovir.
suppositories • Following the
containing an injection of
emollient, brincidofovir,
mesalazine, or ART must be
steroid suspended for
• Analgesia, such at least three
as oral morphine hours due to an
sulfate for penile increase in
edema, ibuprofen, serum
and topical transaminases
lidocaine gel and serum
• Trifluridine eye bilirubin
drops for ocular levels.
lesions and
further scar
prevention
• Maintain clean
lesions to avoid
bacterial
recurrence

Treatment
Guidelines for the recommended treatment of illnesses caused by monkeypox are currently
nonexistent. Since the illness is usually self-limiting and minor, bed rest and supportive therapy can
typically alleviate the patient's suffering (Huang et al., 2022). Antipyretics for fever, analgesics for
pain, and antibiotics for subsequent bacterial infections are examples of supportive care (Durski,
2018). However, hospitalization and expert care can be necessary in extreme circumstances. Antiviral
medications are licensed for the treatment of smallpox and the potential effectiveness of cytomegaly
virus against the MPXV, despite the fact that no commercially accessible medications are available
to treat monkeypox (Reynolds et al., 2017).

Vaccine
There have been three phases in the development of smallpox vaccinations. Smallpox
vaccines were first made by growing the virus on calfskin and then harvesting it from the lymph of
the calf. However, the use of these vaccinations for MPV (mass population vaccination) campaigns
 10

is not authorized at this time. On the other hand, the second version of the smallpox vaccine is made
with more sophisticated and appropriate methods and is grown in tissue cell cultures, which lowers
the risk of infection (Luna et al., 2022).

Furthermore, it has been shown that the presence of replication-competent vaccinia virus in each of
these generations may represent a high risk of unfavorable results. Third-generation smallpox
vaccinations are produced using identical techniques as those of second-generation vaccines. But
because they contain weaker vaccinia viruses with less capacity for reproduction, they provide
increased safety (Moore et al., 2023).

The FDA has authorized the use of second-generation smallpox vaccination ACAM2000 as a
preventative strategy after exposure in emergency scenarios or during smallpox epidemics. Approved
in North America, the MVA-BN vaccine (JYNNEOSTM)was approved after animal testing. It is an
effective and safe choice for avoiding MPV infections in a range of groups, as clinical trials have
shown. Japan and the FDA have authorized LC16. If vaccinated within the first two weeks, serious
illness can be avoided. Studies have shown that immunization against smallpox is more successful in
preventing MPV infection when given promptly. Still, there are currently effective MPXV
vaccinations available. There are three orthopoxvirus vaccines on the market: LC16, JYNNEOS, and
ACAM2000 (Huang et al., 2022).

The FDA authorized ACAM2000 in 2015 for use in the US against monkeypox and smallpox.
From 2015 to 2019, it was the sole vaccination against monkeypox in the nation. ACAM2000 is a
second-generation vaccine made from attenuated vaccinia virus that is replication-competent and
plaque-purified (Berche, 2022). Through numerous skin surface inoculations and a scarification
procedure with a bifurcated needle, it is administered via the skin. Within 28 days of dosing, this
vaccination offers its maximum level of protection. For people exposed to extremely virulent
orthopoxvirus strains, booster injections are advised every three years; for people exposed to less
virulent strains, such as vaccinia virus or cowpox virus, booster doses are advised every ten years. A
third-generation live attenuated non-replicating Ankara vaccine is called MVA-BN. The vaccination
lasts for two weeks after the second dosage and need for another two dosages separated by 28 days.

CONCLUSIONS
In summary, the pathophysiology, history, structure, and transmission of monkeypox
(MPXV) provide important information for the fight against this viral disease. Concerns over
MPXV's potential as a pandemic danger have arisen as a result of the virus's global expansion since
its origin in the Congo Basin. Comprehending the architecture of the virus, namely its shape and
genome, provides insight into its methods of reproduction and interactions with host cells. The
pathophysiology of MPXV highlights the significance of transmission pathways and the demand for
strict preventative measures.

Furthermore, new understandings of the pathophysiology and infection pathways of MPXV

shed light on the disease's clinical signs and its side effects. Due to MPXV's ability to spread through
a variety of pathways, including human-to-human and animal-to-human transmission, extensive
control strategies are essential. Studies in immunology and epidemiology offer vital information for
monitoring and controlling epidemics, directing preventative actions, and creating immunization
plans.

The management of MPXV outbreaks is centered on prevention, which emphasizes the

significance of hygiene measures, isolation techniques, and vaccine efforts. The cornerstone of
treatment for MPXV infections is still supportive care, but further research into antiviral medications
 11

and vaccine development offers hope for better management and preventative measures down the
road. Ultimately, to effectively stop the spread of monkeypox and lessen its effects on international
health, a multidisciplinary strategy combining epidemiological monitoring, immunological insights,
and public health measures is necessary.

REFERENCES
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