What is the mechanism of defense against viral infection?
Viral infection induces an extensive array of defense mechanisms in the host. Innate defenses come into play to block or inhibit initial infection, to protect cells from infection, or to eliminate virus-infected cells, and occur well before the onset of adaptive immunity (Chapter 3).
What is the role of viral evasion in viral infection?
Viruses may also delay or prevent apoptosis induced by CTL within infected cells. Other viral evasion measures aimed at the CD8 T-cell-mediated antiviral defense system serve to inhibit antigen processing, thereby minimizing effector CTL induction.
What happens if you put a virus next to a bacterium?
If you placed a virus next to a bacterium, the virus would be dwarfed. For example, the polio virus is around 50 times smaller than a Streptococci bacterium, which itself is only 0.003mm long. Viruses can be described as either RNA or DNA viruses, according to which type of nucleic acid forms their core.
Why do doctors prescribe antibiotics for viral infections?
Sometimes, in complicated or prolonged viral infections, bacteria may invade as well, and cause what is known as a “secondary bacterial infection”. In these cases, your doctor may prescribe an antibiotic, if one is needed, to kill the specific invading bacteria, but the antibiotic is not being prescribed for your virus.
What is biphasic virus?
A biphasic disease is a disease which has two distinct phases or components. In clinically biphasic diseases, the phases are generally chronologically separated. In histopathologically biphasic tumors (also called biplastic tumors), there is neoplastic tissue which contains two different cellular elements.
Do viruses cause an inflammatory response?
During the earliest stages of a virus infection, cytokines are produced when innate immune defenses are activated. The rapid release of cytokines at the site of infection initiates new responses with far-reaching consequences that include inflammation.
What are the main responses to a viral infection?
The two major divisions of adaptive immunity, antibody and T-cell-mediated, are mainly directed at different targets. Antibodies usually function by binding to free viral particles, and in so doing block infection of the host cell. In contrast, T cells act principally by recognizing and destroying virus-infected cells.
What happens to cells after viral infection?
When the virus is inside the cell, it will open up so that its DNA and RNA will come out and go straight to the nucleus. They will enter a molecule, which is like a factory, and make copies of the virus. These copies will come out of the nucleus to be assembled and receive protein, which protects their DNA and RNA.
What triggers inflammatory response?
The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. The damaged cells release chemicals including histamine, bradykinin, and prostaglandins. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling.
Why does inflammation occur with Covid?
“The antibodies block infection of lung cells, which are where the virus reproduces, but they can also promote infection of immune cells, increasing inflammation,” Lieberman says.
How are viral infections treated?
For most viral infections, treatments can only help with symptoms while you wait for your immune system to fight off the virus. Antibiotics do not work for viral infections. There are antiviral medicines to treat some viral infections. Vaccines can help prevent you from getting many viral diseases.
How does the immune system response to bacterial and viral infections?
The body reacts to disease-causing bacteria by increasing local blood flow (inflammation) and sending in cells from the immune system to attack and destroy the bacteria. Antibodies produced by the immune system attach to the bacteria and help in their destruction.
Why can't antibiotics be used to treat a virus How are viruses treated?
Antibiotics cannot kill viruses because bacteria and viruses have different mechanisms and machinery to survive and replicate. The antibiotic has no “target” to attack in a virus. However, antiviral medications and vaccines are specific for viruses.
What happens during a viral infection?
Viruses infect a host by introducing their genetic material into the cells and hijacking the cell's internal machinery to make more virus particles. With an active viral infection, a virus makes copies of itself and bursts the host cell (killing it) to set the newly-formed virus particles free.
Why do antiviral medications often have side effects quizlet?
Antiviral drugs tend to have significant adverse effects on the host because they alter viral interaction within the host cell.
What effects do viruses have on cells?
Effects on Cell Biochemistry: Many viruses inhibit the synthesis of host cell macromolecules, including DNA, RNA, and protein. Viruses may also change cellular transcriptional activity, and protein-protein interactions, promoting efficient production of progeny virus.
How do viral infections affect HSPCs?
The first two mechanisms act viadirect effects on HSPCs: (1) direct viral infection or (2) viral recognition by HSPCs. The other two mechanisms are indirectly: (3) viainflammatory mediators or (4) through changes in the BM microenvironment. During a viral infection, more than one of these mechanisms contribute to alterations in hematopoiesis, as they are also likely to influence each other, as indicated by the gray arrows. This is exemplified by the fact that (A)when a virus infects an HSPC, it is generally also recognized through intracellular PRRs, (B)recognition of viral infections by HSPCs usually also leads to the production of pro-inflammatory cytokines, such as type I IFNs, and (C)production of IFNγ by virus-specific T cells can directly affect HSPCs but can also induce IL-6 production by MSCs, thereby enhancing myeloid differentiation. Better understanding of the complex interactions between these different mechanisms will be important to adequately treat or prevent anemia and BM failure in patients with viral infections. (The illustrations used to generate this figure are gratefully obtained from the Powerpoint Image Bank of Servier Medical Art).
How do viruses start?
Viral infections start with local invasion, for example of an epithelial or mucosal barrier. Once the virus manages to overcome the early mechanical barriers, such as cilia, mucus, or skin integrity and infects a target cell, innate immune mechanisms come into play to contain the infection. As an example, during influenza virus infection, viral RNA present within infected cells is recognized by pathogen recognition receptors (PRRs), which leads to the secretion of type I interferons (IFNs), pro-inflammatory cytokines, eicosanoids, and chemokines. Type I IFNs stimulate the expression of hundreds of genes [IFN-stimulated genes (ISGs)] in neighboring cells, which induce an antiviral state. Pro-inflammatory cytokines and eicosanoids cause local and systemic inflammation, induce fever and anorexia, and instruct the adaptive immune response. Chemokines recruit additional immune cells, including neutrophils, monocytes, and natural killer cells to the airways. Virally infected epithelial cells become the target of NK cells. Monocytes and neutrophils help to clear infected dead cells, thus contributing to viral clearance (8). If the virus establishes infection despite these defenses, the ultimate clearance of the virus requires adaptive immunity, which relies on virus-specific antibodies and T cells. As an example, T cell responses against influenza comprise perforin/granzyme-induced lysis and tumor necrosis factor receptor family dependent apoptosis of infected cells and production of pro-inflammatory and regulatory mediators, such as IFNγ (9). In some cases, a strong antiviral response can even be more destructive than the virus itself and contribute to viral persistence (10–12).
How does stress affect hematopoiesis?
Stress-induced hematopoiesis has most likely evolved to provide the body with the appropriate type(s) of blood cells to combat the invading pathogen. Signals originating from the infectious agent or the ensuing immune response can compel HSCs to change from a quiescent into a proliferative state and dictate the differentiation pathways of hematopoietic progenitors (13) . For example, inflammation induced by immunization or LPS injection increases the production of granulocytes, macrophages, and dendritic cells but decreases the production of B cells (14, 15). Interestingly, the response of the hematopoietic system to bacterial products can also be influenced by non-immune cells, as BM stromal cells and endothelial cells can translate pathogenic information to lineage-specific differentiation through the production of pro-inflammatory cytokines or chemokines (16, 17). Macrophages also play an important role in the BM in regulating myelopoiesis, both during the steady state and upon inflammation, as was reviewed by McCabe and MacNamara (18). Inflammatory mediators, such as interferon-γ (IFNγ), skew the differentiation of hematopoietic stem and progenitor cells (HSPCs) toward monocytes at the expense of other lineages, as we reviewed previously (19). Boosting myelopoiesis during infections while inhibiting other lineages is probably related to the fact that myeloid cells are short lived, have little ability to expand in the periphery, and are rapidly consumed during acute bacterial infections. However, monocytes and granulocytes are not essential for the clearance of a viral infection, whereas lymphocytic cells, such as NK cells and T cells do have an important role in the immune response against viruses. Therefore, it is conceivable that significant differences exist in hematopoietic output upon an infection with a bacterial versus viral pathogen. In the coming section, we will discuss non-pathogenic and pathogenic outcomes of viral infections on BM output, and then, we will elaborate on four distinct effects by which viral infections can modulate the hematopoietic process.
How do blood cells develop?
All blood cells develop from a small subset of the same progenitor cells in the bone marrow (BM) through a process called hematopoiesis. Hematopoietic stem cells (HSCs) give rise to red and white blood cells and platelets, and this hematopoietic process is tightly regulated to ensure both a balanced output of the different blood cells and a lifelong maintenance of self-renewing HSCs (1). The contribution of individual HSCs to blood cell production under steady state conditions is low, as this is mainly governed by multipotent progenitors with less or no self-renewing capacity (2). HSCs only occasionally give rise to new progenitors and are instead protected and nurtured by a complex microenvironment of resident hematopoietic and non-hematopoietic cells (3). This BM niche produces factors that maintain the quiescence, self-renewal, and survival of the HSCs. However, upon stress induced by cytotoxic damage, transplantation, inflammation, or infection, the pool of quiescent HSCs is activated and required to actively contribute to the hematopoietic process (4).
How many different types of viruses are there?
Viruses that can infect humans range in size from 20 to 260 nm, are estimated to be of at least 30 different types and can cause pathologies, ranging from respiratory manifestations, enterocolitis, meningitis, encephalitis, hepatitis, and sexually transmitted diseases. Structurally, viruses are composed of a protein capsid that protects their genomic material and, in some cases, facilitates entry into the host cell. Some viruses can also be surrounded by a lipid bilayer – enveloped viruses, which also contain membrane glycoproteins that can interact with entry receptors on the surface of the host cells. The genome of viruses can be composed of DNA or RNA. RNA genomes can be coding, much like an mRNA molecule (positive-strand RNA) or have a complementary RNA molecule (negative-strand) that needs to be copied into a positive strand, which can then be translated by the cellular machinery. DNA viruses can have a single-stranded or double-stranded genome. The conformation of the genome can be linear or circular, and continuous or segmented. RNA genomes are limited by the inherent instability of RNA and usually contain fewer genes, with the smallest virus containing 3–4 genes. DNA genomes are generally bigger and might encode up to 200 genes. The size of the genome will impact the dependence of the virus on the cellular replication machinery and will also impact on how good the virus is in escaping immune responses. Bigger genomes are able to encode a broader range of sophisticated immune-evasion mechanisms (7).
What are the receptors that detect pathogens?
Pathogen recognition receptors are receptors that detect pathogen-associated molecular patterns (PAMPs) within the body (48, 49). PRRs include toll-like receptors, retinoic acid-inducible gene 1 (RIG-I)-like receptors (RLRs), and cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) (50). Four TLR members seem to play a critical role in recognition of viral nucleic acids: TLR3 recognizes dsRNA (dsRNA constitutes the genome of one class of viruses but is also generated during the life cycle of many viruses), TLR7 and 8 recognize single-stranded RNA (ssRNA), and TLR9 responds to dsDNA viruses recognizing non-methylated viral CpG-containing DNA. Although the majority of TLRs sense pathogen components on the cell surface, TLR3, TLR7, TLR8, and TLR9 sense nucleic acids in endosomal compartments. Other TLRs are also involved in viral recognition; TLR2 and TLR4 were shown to detect viral components such as envelope glycoproteins (51) and other components of viruses such as HIV, HBV, vaccinia virus (VV), and Dengue (52–55).
Can a virus infect HSPCs?
It has been described that a number of viruses including, CMV, Hepatitis C virus (HCV), and human herpes viruses can directly infect HSPCs (38–41). For some of these viruses, it has been documented that they can suppress hematopoiesis after direct infection of HSPCs. For example, Simmons et al. demonstrated that CMV infection can mediate myelosuppression in vitro(42). Furthermore, human herpes viruses 7 (HHV7) has the potential to infect HSPCs as well as impair HSPC survival and proliferation, presumably vialysis, or induced cell death (41). Parvovirus B19, the only known human pathogenic parvovirus, has a selective tropism for the erythroid lineage in the BM, where productive infection induces a block in erythropoiesis that can be manifested as a transient or persistent erythroid aplasia (43).
Why are viruses so difficult to kill?
Viruses pose a considerable challenge to the body’s immune system because they hide inside cells. This makes it difficult for antibodies to reach them. Some special immune system cells, called T-lymphocytes, can recognise and kill cells containing viruses, since the surface of infected cells is changed when the virus begins to multiply. Many viruses, when released from infected cells, will be effectively knocked out by antibodies that have been produced in response to infection or previous immunisation.
How does an antibiotic work?
Serious infections can be treated with antibiotics, which work by disrupting the bacterium’s metabolic processes, although antibiotic-resistant strains are starting to emerge. Immunisation is available to prevent many important bacterial diseases such as Hemophilus influenza Type b (Hib), tetanus and whooping cough..
What is the name of the bacteria that are shaped like tiny spirals?
Spirochaetes – as the name suggests, these bacteria are shaped like tiny spirals. Spirochaetes bacteria are responsible for a range of diseases, including the sexually transmissible infection syphilis.
How do viruses spread?
Viruses are spread from one person to another by: Bacteria types. Characteristics of the bacterium. Curing a bacterial infection. Virus types. The body’s response to viral infection. Curing a viral infection. Immunisation against viral infection is not always possible. Where to get help.
Why are antibiotics useless?
Antibiotics are useless against viral infections. This is because viruses are so simple that they use their host cells to perform their activities for them. So antiviral drugs work differently to antibiotics, by interfering with the viral enzymes instead.
What causes infections in humans?
Where to get help. Things to remember. Many human infections are caused by either bacteria or viruses. Bacteria are tiny single-celled organisms, thought by some researchers to be related to plants. They are among the most successful life forms on the planet, and range in habitat from ice slopes to deserts.
Why are viruses bad for the body?
Viruses pose a challenge to the body’s immune system because they hide inside cells.
Why can't you use antibiotics for viral infections?
You may be told you cannot use an antibiotic for a viral infection because they are ineffective and may lead to “antibiotic resistance”. Why don’t antibiotics kill viral infections, and how can overuse of an antibiotic lead to “antibiotic resistance”? Antibiotics cannot kill viruses because viruses have different structures ...
What to do if you have a viral infection?
If you come down with a viral illness, you should rest, drink plenty of fluids and treat symptoms such as fever or aches and pains. Treatment options include proper doses of pain and fever relievers like over-the-counter (OTC) acetaminophen or ibuprofen, or as directed by your doctor. If you are diagnosed with a viral illness such as a cough, cold or sore throat, and your symptoms worsen or do not clear up within 10 days, be sure to contact your doctor.
How are viruses different from bacteria?
Viruses are structurally different from bacteria. Viruses live and replicate inside of a human cell and they cannot live outside of this environment. Viruses insert their genetic material into a human cell’s DNA in order to reproduce.
How do antibiotics fight back against drugs?
Bacteria fights back against a drug in many ways: by strengthening their own cell walls. by producing enzymes that can inactivate the antibiotic.
How long does it take to treat a UTI?
For example, for uncomplicated UTI in women, fosfomycin is a medicine that can be given in one single dose, but trimethoprim–sulfamethoxazole (Bactrim, Septra) is given as a 3-day course.
What infections does ACP treat?
The treatment advice from ACP centers on uncomplicated and common infections like bronchitis / COPD, pneumonia, urinary tract infection (UTI), and skin infections (cellulitis) in otherwise healthy patients .
When does antibiotic resistance occur?
In general terms, antibiotic resistance can occur when bacteria learn to “fight off” the antibiotic.
How can a viral infection be transmitted?
Also, similarly to bacterial infections, viral infections can be transmitted by the bite of an infected insect or through consuming food or water that has been contaminated.
What is the definition of close contact with a person who has a bacterial infection?
close contact with a person who has a bacterial infection, including touching and kissing. contact with the body fluids of a person who has an infection, particularly after sexual contact or when the person coughs or sneezes. transmission from mother to child during pregnancy or birth.
Is my stomach bug bacterial or viral?
When you experience symptoms like nausea, diarrhea, or abdominal cramps, you likely have a stomach bug. But is it due to a viral or bacterial infection?
Why is it dangerous to take antibiotics?
This is dangerous because over-prescribing antibiotics can lead to antibiotic resistance. Antibiotic resistance occurs when bacteria adapt to be able to resist certain antibiotics.
What is antibiotic resistance?
Antibiotic resistance occurs when bacteria adapt to be able to resist certain antibiotics. It can make many bacterial infections more difficult to treat. If you’re prescribed antibiotics for a bacterial infection, take your entire course of antibiotics — even if you begin to feel better after a couple of days.
How can bacteria be transmitted?
In addition to being transmitted from person to person, bacterial infections can also be transmitted through the bite of an infected insect. Additionally, consuming contaminated food or water can also lead to an infection.
Why do we stay home when we are sick?
Stay home if you’re ill to help prevent transmitting your infection to other people.
What is the pro-inflammatory state of HIV?
A pro-inflammatory state was described since the beginning of the HIV pandemic, which includes higher serum levels of IL-6, TNF-α, TGF-β, and other inflammatory molecules [36]. Additionally to the immune system aging (known as “inflamm-aging”), those who live with HIV becomes more vulnerable to a chronic inflammatory state that can lead to some diseases [37], including renal dysfunction.
What are the most likely scenarios for HIV-associated kidney disease?
Three major scenarios are more likely in HIV-associated kidney disease: HIV-associated nephropathy (HIVAN), HIV-associated immune complex kidney disease (HIVICK), and thrombotic microangiopathy. HIVAN usually happens in the late stages of HIV infection with or without acquired immunodeficiency syndrome (AIDS). Some APOL1polymorphisms may suggest a higher risk for HIVAN [38,42]. Management of HIVICK remains unclear [38], as the pathophysiology of thrombotic microangiopathy in HIV [43], but some studies have shown that HIV is highly associated with thrombotic thrombocytopenic purpura [44-46] or, less frequently, hemolytic uremic syndrome [47].
How many people died from HBV in 2015?
HBV infection is of global public health concern. In 2015, the WHO estimated 257 million HBV-infected individuals around the world and approximately 887,000 people died from HBV-related liver disease by that year [54]. Nearly 250 to 350 million people (5% of the world’s population) are chronically HBV-infected, which makes HBV to be one of the most common human pathogens. Additionally, 3% to 5% of the patients with chronic HBV infection may develop kidney disease as a complication [55].
What is the role of NLRP3 in fibrosis?
The NLRP3 inflammasome plays different roles in the pathogenesis of renal fibrosis as it mediates the inflamma tory response and it also promotes pyroptosis, mitochondrial regulation, and myofibroblast differentiation [3]. NLRP3 activation in renal diseases aggravates inflammation, as well as the consequent fibrosis.
Which cells are involved in the inflammatory mechanisms that underlies acute kidney injury?
The podocytes, resident visceral epithelial cells that constitute the glomerulus, can express all the inflammasome components of NLRP3 that seems to be involved in the inflammatory mechanisms that underlies acute kidney injury (AKI) and chronic kidney disease (CKD) [2,3].
Can viral infections cause kidney failure?
In general, viral infections can cause many kidney diseases, which diagnosis depend on clinical and laborator y investigations, as well as histological analysis. Many mechanisms are involved, including viral kidney tropism, induction of abnormal immune complexes, direct cytopathic effects, and multiorgan failure [31]. SARS-CoV-2 infection can trigger glomerular diseases (several types were reported, including collapsing glomerulopathy) or aggravate a pre-existing disease [23,32].
Is NLRP3 inflammasome dependent?
It is now known that NLRP3 has several inflammasome-dependent and independent functions in the kidney. The inflammasome-dependent NLRP3 mediates the progression of kidney diseases by escalating local kidney inflammatory response and promoting a crosstalk between the immune cells and the nonimmune renal cells. On the other hand, the inflammasome-independent NLRP3 regulates tubular epithelial cells apoptosis [3].
What is the endotoxin of bacteria?
Bacterial endotoxin is characterized by all the following:#N#A. Consists of LPS.#N#B. Determines bacterial shape. #N#C. May have different effects depending on the specific bacterial source.#N#D. Is toxic due to the effects of the polysaccharide side chains.#N#E. A and C.
Which two genera are responsible for the formation of C. coli?
C. are formed by members of the genera Clostridium and Bacillus.
What does growth mean in microbiology?
A. In microbiology, growth usually refers to an increase in size of the bacteria.
Do drugs that target prokaryotic protein synthesis have any effect on eukaryotic cell growth?
C. Drugs that target prokaryotic protein synthesis would have no effect on eukaryotic cell growth.
How did epidemiologists study disease?
A. Previous to this study epidemiologists studied disease by examining death certificates
Do genes cause high blood pressure?
A. Genes play little or no role in contributing to high blood pressure.