Nonspecific Defenses Against Infection

1. Explain what is meant by nonspecific defense and list the nonspecific lines of defense in the vertebrate body.
Nonspecific defense is a trait of innate immunity, they quickly recognize and respond to a broad range of
microbes regardless of their precise identity. These nonspecific lines of defense include:
External: Skin, Mucous membranes, Secretions
Internal: Phagocytic Cells, Antimicrobial proteins, Inflammatory response, and Natural Killer Cells

2. Distinguish between:
a. innate and acquired immunity
Innate immunity: Is present before any exposure to pathogens and is effective from the time of birth. These
defenses are largely nonspecific, and quickly recognize and respond to a broad range of microbes regardless of
their precise identity. These nonspecific lines of defense include:
External: Skin, Mucous membranes, Secretions
Internal: Phagocytic Cells, Antimicrobial proteins, Inflammatory response, and Natural Killer Cells
Acquired Immunity: develops only after exposure to inducing agents such as microbes, abnormal body cells,
toxins or other foreign substances. They are highly specific, that is they can distinguish one inducing agent from
another, even if they only differ slightly. This is achieved by white blood cells called LYMPHOCYTES, which
produce two general types of immune responses. Humoral (antibodies) and Cell-mediated (cytotoxic
lymphocytes)
b. humoral and cell mediated response
Humoral response: Cells derived from B lymphocytes secrete defensive proteins called ANTIBODIES that bind to
microbes and mark them for elimination.
Cell Mediated response: Cytotoxic lymphocytes directly destroy infected body cells, cancer cells and foreign
tissue.

3. Explain how the physical barrier of skin is reinforced by chemical defenses.

Intact skin is a barrier that can’t usually be penetrated. Coupled with the mucous membranes lining the
digestive, respiratory and genitourinary tracts bar the entry of potentially harmful microbes. Certain cells in the
mucus membrane produce MUCUS, a viscous fluid that traps microbes and other particles. Microbial colonization
is also inhibited by the washing action of the mucous secretions of saliva and tears. Together they provide an
environment hostile to microbes.
Oil and Sweat glands give the skin a pH ranging from 3 to 5 which is acidic enough to prevent colonization of
many microbes. Similarly the acidic environment of the stomach destroys most pathogens before they can enter
the intestines.
Secretions from the skin and mucus membanes also contain antimicrobial proteins. One such protein is
LYSOZYME, an enzyme that digests the cell walls of many bacteria. Present in saliva, tears and mucus
secretions.
In addition microbes that penetrate the bodies external defenses must contend with the bodies internal
mechanism of innate defense. These defenses primarily depend on PHAGOCYTOSIS.

4. Define phagocytosis. Name four types of phagocytic leukocytes.

Phagocytosis: the ingestion of invading microorganisms by certain types of white blood cells generically referred
to as PHAGOCYTES. These Phagocytes produce certain antimicrobial proteins and help initiate inflammation
which can limit the spread of microbes in the body.
Phases of Phagocytosis:
1) Phagocytes engulfs microbe
2) A vacuole is formed which fuses with a lysosome
3) Nitric oxide and toxic forms of oxygen poison the microbe
4) lysozyme degrades the microbial componets

4 types of phagocytic leukocytes: Neutrophils, macrophages, Eosinophils, dendritic cells

Neutrophils:
-Constitute about 60%-70% of all white blood cells.
-Are attracted to and then enter infected tissue, ENGULFING and DESTROYING the microbes there
-Tend to self destruct in the process of phagocytosis, avg. life span is only a few days
Macrophages (big eaters):
-Large, long lived cells develop from MONOCYTES
-Constitute about 5% of circulating blood cells.
-Circulate in the blood for a few hours before they migrate into tissues, where they become macrophages
-Carrying out phagocytosis sets off internal signaling pathways that activate the macrophages, increasing their
 defensive abilities
-Permanent residents in the spleen, lymph nodes, and other tissues of the lymphatic system.
Eosinophils:
-have low phagocytic activity, but critical to defense against multicellular parastic invaders (like blood fluke)
-rather then engulfing, eosionphils position themselves against the parasites body and then discharge
destructive enzymes that damage the invader.
Dendritic Cells:
-can ingest microbes like macrophages do
-primary role is to stimulate the development of acquired immunity.

5. Explain how interferon limits cell-to-cell spread of viruses.

Two types of interferon (a & B) provide innate defense against viral infections.
They are secreted by virus infected body cells and induce neighboring uninfected cells to produce other
substances that inhibit viral reproduction.

6. Describe the inflammation response, including how it is triggered.

Damage to tissue by physical injury or the entry of pathogens leads to the release of chemical signals that trigger
a the localized INFLAMMATORY RESPONSE.
When injured, MAST CELLS found in connective tissues release HISTOMINE(one of the most active chemicals)
that triggers dialation and increased permeability of nearby capillaries.
– Histamine released from mast cells in connective tissue
– Prostaglandins released from activated macrophages increases blood flow to injured area
– Blood-filled capillaries leak blood causing redness and swelling
– Enhanced blood flow and vessel permeability help deliver antimicrobial proteins and blood clotting
elements
• Blood clotting begins the healing and isolates the microbe
– Activated complement proteins modulate release of histamine or chemoattractants for
macrophages
– Chemokines direct phagocyte migration and stiumlate production antimicrobial compounds

7. Describe the factors that influence phagocytosis during the inflammation response.
Injured cells put out a call for reinforcements, secreting chemicals that stimulate the release of additional
neutrophils from the bone marrow.
Moderate fevers may facilitate phagocytosis and, by speeding up body reactions hasten the repair of tissues.

8. Explain how the action of natural killer cells differs from the action of phagocytes.
Surface receptors on the NK cell recognize general features on the surface of its targets. Once it is attached to a
virus infected cell or cancer cell, the NK cell releases chemicals that lead to the death of the striken cell by
APOPTOSIS, or programmed cell death.

9. Explain what occurs during the condition known as septic shock.

Certain bacterial infections can induce an overwhelming systemic inflammatory response. It is characterized by
high fever and low blood pressure.

10. Describe the roles of antimicrobial proteins in innate immunity.

In addition to lysozyme. Other antimicrobial proteins include about 30 serum proteins that make up the
COMPLEMENT SYSTEM. In the absence of an infection, these proteins are inactive. Substances on the surface of
many microbes however can trigger a cascade of steps that activate the complement systems. Leading to
lysis(bursting) of invading cells. Certain complacent proteins also help trigger inflammation or play a role in
acquired defense.

***Concept Check 43.1***

1) Innate defenses are nonspecific. How, then, do macrophages recognize an infectious agent, such as a bacterium
Macrophages have receptors that bind to polysaccharides present on the surface of bacterial cells but not on body
cells.
2) What causes the common signs of inflammation, redness, swelling and heat, and how do these changes help protect the
body against infection
Vessel dilation, which allows enhanced blood flow, and increase vessel permeability result in the common signs of
inflammation. These vascular changes aid in delivering clotting factors, antimicrobial proteins, and phagocytic
cells to the tissue of the affected region. All of these help in repairing tissue damage and stopping the spread of
infection.
3) State two ways in which the innate defenses of insects (invertebrates) and vertebrates are similar.
 The exoskeleton of insects provides an external barrier similar to the skin and mucous membranes of vertebrates.
Phagocytic cells and antimicrobial proteins also contribute to innate defenses in both insects and vertebrates.

How Specific Immunity Arises

11. Distinguish between antigens and antibodies.

Antibodies: are released during the Humoral response and are secreted by B lymphocytes, and bind to microbes
and mark them for elimination.
Antigens: is any foreign molecule that is specifically recognized by lymphocytes and elicits a response from them.

12. Distinguish between antigen and epitope.

A lymphocyte actually recognizes and binds to just a small, accessible portion of an antigen called an EPITOPE. A
single antigen usually has several different epitopes, each capable of inducing a response from lymphocytes that
recognize that epitope.

13. Explain how B lymphocytes and T lymphocytes recognize specific antigens

B cells and T cells recognize antigens by means of antigen specific receptors embedded in their plasma
membranes. A single B or T cell bears about 100,000 of these ANTIGEN RECEPTORS, and all the receptors on a
single cell are identical, that is they all recognize the same epitope. In other words, each lymphocyte displays
specifically for a particular epitope on an antigen and defends against that antigen or a small set of closely
related antigens.

14. Explain how the particular structure of a lymphocyte’s antigen binding site forms during development. Explain the role of
recombinase in generating the staggering variability of lymphocytes.
--Newly formed lymphocytes are all alike, but later develop into T cells or B cells depending on WHERE they
continue their maturation.
--Lymphocytes that migrate from bone marrow to the THYMUS(a gland in the thoracic cavity above the heart)
develop into T cells
--Lymphocytes that remain in the bone marrow and complete maturation become B cells
--The variable regions at the tip of each antigen receptor chain, which form the antigen binding site, account for
the diversity of lymphocytes. Each person has about 1 million different B cells and 10 million different T cells,
each with a particular antigen binding specificity. Thus can respond to an enormous number of different antigen
receptor chains.

15. Explain why the antigen receptors of lymphocytes are tested for self-reactivity during development. Predict the consequences
that would occur if such testing did not take place.
Because the rearrangements of antigen receptor genes are random, a developing lymphocyte may end up with
antigen receptors that are specific for some of the bodies own molecules. Thus their antigen receptors are
tested for potential self reactivity. If they are, they are either destroyed by apoptosis or rendered nonfunctional.
Failure to eliminate them and maintain SELF TOLERENCE can lead to autoimmune diseases.

16. Describe the mechanism of clonal selection. Distinguish between effector cells and memory cells.
Clonal Selection: Each antigen, by binding to specific receptors, selectively activates a tiny fraction of cells from
the bodys diverse pool of lymphocytes; this relatively small number of selected cells gives rise to clones of
thousands of cells, all specific for and dedicated to eliminating that antigen.
This cloning results in 2 type of cells.
One clone consist of a larger number of short lived EFFECTOR CELLS that combat the same antigen. The other
clone consists of MEMORY CELLS, long lived cells bearing receptors specific for the same inducing antigen.

17. Distinguish between primary and secondary immune responses.

Primary immune response is a result of the first time a body is exposed to a certain antigen. In this stage B cells
generate antibody secreting effecter B cells, called PLASMA CELLS, and selected T cells are activated in their
effecter forms.
If an individual is exposed again to the same antigen, the response is faster and of greater magnitude and more
prolonged. This is SECONDARY IMMUNE RESPONSE

18. Describe the cellular basis for immunological memory.

The immune systems capacity to generate secondary immune responses called IMMUNOLOGICAL MEMORY ,
depends on the clones of long lived T and B memory cells generated following initial exposure to an antigen.

19.

20. Compare the structures and functions of cytotoxic T cells and helper T cells.
Class 1 MHC molecules displaying bound peptide antigens are recongnized by CYTOTOXIC T Cells
 Class 2 MHC molecules including Dendritic, macorphages and B cells known as Antigen presenting cells displayed
internalized antigens to T HELPER CELLS.
The T cell receptor binds with an MHC molecule peptide antigen complex.

21. Compare the production and functions of class I MHC and class II MHC molecules.
Class I MHC: found on almost all nucleated cells of the body, bind peptides derived from foreign antigens that
been synthesized within the cell.
Class 2 MHC: are made by just a few cell types, mainly dendritic cells, macrophages and B cells. In these cells
class 2 MHC bind peptides derived from foreign materials that been internalized and fragmented through
phagocytosis or endocytosis.

***Concept Check 43.2***

1) Draw a B cell receptor, and label the following light chaings, heavy chains, disulfide bridges, variable V regions constant C
regions, antigen binding sites, Transmembrane region, and cytoplasmic tails. How does the structure of a secreted
antibody differ?
See figure 43.8a; a secreted antibody lacks a transmembrane region and cytoplasmic tail.
2) What is the major difference in the types of antigens bound by B cell receptors and T cell receptors
B cell receptors bind intact extracellular antigens present on the surface of microbes or free in body fluids. T cell
receptors bind small fragments of antigens that are complexed with class I or class II mHC molecules on the
surface of infected body cells or antigen presenting cells, respectively.
3) Consider the process of clonal selection of B cells show in Figure 43.12. How does this process demonstrate both the
specificity and memory of acquired immunity.
Specificity: Only B cells with receptors that bind to the antigen are selected to proliferate and differentiate into
plasma cells secreting antibodies specific for the antigen and memory B cells bearing receptors specific for the
same antigen. Memory: the large number of memory B cells generated respond more rapidly to the same antigen
the next time it enters the body.
4) A light chain immunoglobulin gene consists of 40 V gene segments and 5 J gene segments and a heavy chain gene consists
of 51 V gene segments and 6 J gene segments and another set of gene segments D, of which there are 27. How many
different antigen binding specificities can be generated given random V-J and VDJ arrangements.
40 V X 5 J = 200 possible light chains. 51 V X 6 J X 27 D = 8,262 possible heavy chains. Each antigen binding site
is fromed from a region on a light chain and heavy chain. The number of possible random combinations is 200 ligh
chains X 8,262 heavy chains = 1.65 X 10^6 possible antigen binding specificities.

Immune Responses

22. Distinguish between humoral immunity and cell-mediated immunity.

Acquired immunity includes two branches, HUMORAL and CELL MEDIATED immunity.
Humoral Immunity: involves the activation and clonal selection of B cells, resulting in production of secreted
antibodies that circulate in the blood and lymph
Cell Mediated Immunity: involves the activation and clonal selection of cytotoxic T cells, which directly destroy
certain target cells.

23. Describe the roles of helper T lymphocytes in both humoral and cell-mediated immunity.
When a helper T cell encounters and recognizes a class II MHC molecule-antigen complex on an antigen present
cell, the helper T cell proliferates and differentiates into a clone of activated helper T cells and memory helper T
cells.
--Activated helper T cells secrete several different cytokines that stimulate other lymphocytes, thereby
promoting cell mediated and humoral responses.
--Dendritic cells are particularly effective in presenting antigens to naïve helper T cells, dendritic cells are
important in triggering a primary immune response.
--Macrophages play the key role in initiating a secondary immune response by presenting antigens to memory
helper T cells
--B cells primarily present antigens to helper T cells in the course of the humoral response.

24. Describe the functions of the proteins CD4 and CD8.

Both Are Surface Proteins
CD4 is present on most helper T cells, and binds the class II MHC molecule. This interaction helps keep the
helper T cell and the antigen presenting cell joined while activation of the helper T cell proceeds.
CD8 is present on most cytotoxic T cells, and greatly enchances the interaction between a target cell and a
cytotoxic cell. Binding of CD8 to the side of a class I MHC molecule helps keep the two cells in contact during
activation of the cytotoxic T cell.

25. Explain how cytotoxic T cells and natural killer cells defend against tumors.
 Because tumor cells carry distinctive molecules(tumor antigens) not found on normal body cells, they are
identified as foreign by the immune system. Class I MHC molecules on a tumor cell display fragments of tumor
antigens to cytotoxic T cells. NK cells as part of the body’s non specific innate defenses, can induce apoptosis in
virus infected and cancer cells.

26. Distinguish between T-dependent antigens and T-independent antigens.

Antigens that induce antibody production only with assistance from helper T cells are known as T DEPENDENT
ANTIGENS.
Some antigens however can evoke a B cell response without involvement of helper T cells. There are T
INDEPENDENT ANTIGENS and include the polysaccharides of many bacterial capsules and the proteins that make
up bacterial flagella.

27. Explain why macrophages are regarded as the main antigen-presenting cells in the primary response but memory B cells are
the main antigen-presenting cells in the secondary response.
Macrophages are the main antigen presenting cells in the primary response because it is the first time the body
is exposed to the antigen. The body secretes various effecter cells including plasma cells, which mark and
eventually destroy the antigens. Due to clonal selection, during secondary response the long lived clones of
memory B cells produce clones of themselves to fight the antigen faster.

28. Explain how antibodies interact with antigens.

Antibodies bind to antigens(to mark for elimination), this is also the basis of several antigen disposal
mechanisms.

29. Diagram and label the structure of an antibody and explain how this structure allows antibodies to (a) recognize and bind to
antigens, and (b) assist in the destruction and elimination of antigens.
See figure 43.18

30. Distinguish between the variable (V) and constant (C) regions of an antibody molecule.
Variable (V): Are at the tips of the Y(in b cells) are light and heavy chain variable (v) named because their amino
acid sequences vary extensively from one b cell to anoter.
Constant (C): the remainder of the molecule is made up of constant (c) whose amino acid sequences vary little
from cell to cell.

31. Describe the production and uses of monoclonal antibodies.

Monoclonal antibodies are prepared from a single clone of B cells grown in culture, all of which are identical and
specific for the same epitope on an antigen. In both basic research and medical applications, monoclonal
antibodies are particularly useful for tagging specific molecules. For example, certain types of cancer are treated
with tumor specific monoclonal antibodies bound to toxin molecules. The toxin linked antibodies carry out a
precise search and destroy mission, selectively attaching to an killing tumor cells.

32. Compare the processes of neutralization, opsonization, and agglutination.

These are all Antigen disposal mechanisms.
The simplest VIRAL NEUTRALIZATION antibodies bind to certain proteins on the surface of a virus, thereby
blocking the virus’s ability to infect a host cell.
Similarly antibodies may bind to a pathogenic bacterium, coating much of the bacterial surface. In a process
called OPSONIZATION, the bound antibodies enhance macrophage attachment to the microbes and thus increase
phagocytosis.
Antibody mediated AGGLUTINATION (clumping) of bacteria or viruses forms aggregates that can be readily
phagocytosed by macrophages. Agglutination is possible because each antibody molecule has at least two
antigen binding sites that can bind to identical epitopes on separate bacterial cells or virus particles linking them
together.

Immunity in Health and Disease

33. Distinguish between active and passive immunity and describe examples of each.
Immunity conferred by natural exposure to an infectious agent is called ACITVE IMMUNITY because it depends
on the action of a person’s own lymphocytes and the resulting memory cells specific fro the invading pathogen.
Active Immunity also can develop following immunization often called vaccination. This Vaccination induce an
immediate immune response and long lasting immunological memory(thanks to memory cells) (Ex. Smallpox)
Immunity can also be conferred by transferring antibodies from an individual who is immune to a particular
infectious agent to someone who is not. This Is called PASSIVE IMMUNITY, because it does not result from the
action of the recipients own B and T cells. Instead the transferred antibodies are poised to immediately help
 destroy any microbes for which they are specific. It provides immediate protection, but persists only as long as
the transferred antibodies last. (ex. Rabies)

***Concept Check 43.3***

1) Describe the main role of each of the following cell types, once it is activated by antigens and cytokines: helper T
cells, cytotoxic T cell and B cell
An activated helper T cell secretes cytokines that promote activation of both cytotoxic T cells and B cells. An
activated cytotoxic T cell kills infected cells and tumor cells by apoptosis. An activated B cell differentiates
into plasma cells that secret antibodies
2) What cells and functions would be deficient in a child born without a thymus?
A child lacking a thymus would have no functional T cells. Without helper T cells to help activate B cells, the
child would be unable to produce antibodies against extracelluar bacteria. Without cytotoxic T cells or helper
T cells to help activate them, the childs immune system would be unable to kill virus infected cells
3) Discuss how antibodies help protect us from infection or the effects of infection
Antibodies bound to viruses can block their attachment to potential host cells (viral neutralization) coating of
bacteria or other particles by antibodies bound to surface antigens increases their phagocytosis by
macrophages (opsonization) Antibodies bound to antigens on bacterial cells also can activate a cascade of
complement proteins leading to lysis of the bacteria (complement activation) Cross linking of antigens on
many bacterial cells or viruses by binding of multiple antibody molecules can lead to formation of large
clumps (agglutination) which are then phagocytosed.
4) Explain why passive immunization provides short term protection from an infection, whereas active immunization
provides long-term protection
Passive immunization the transfer of antibodies from one individual to another is protective only as long as
the antibody molecules last. Active immunization, the introduction of antigen, induces an immune response
in the recipient that can lead to the generation of long lived memory cells. Someone who is actively
immunized may be immune to that antigen for life.

34. Explain how the immune response to Rh factor differs from the response to A and B blood antigens.
Blood group (A, B) antigens and related bacterial epitopes are polysaccharides. Such polysaccharide antigens
induce immune responses in which no memory cells are generated.
Rh factor, as a protein antigen induces immune responses in which memory cells are generated. Later exposure
of these memory cells to the Rh factor leads to production of anti-Rh antibodies that are IgG.

35. Describe the potential problem of Rh incompatibility between a mother and her unborn fetus and explain what precautionary
measures may be taken.
An Rh-negative mother who carries an Rh positive fetus can be dangerous. If small amounts of fetal bloo cross
the placenta, the moth mother mounts a humoral response against the Rh factor. To prevent this the mother is
injected with anti Rh antibodies around the 7th month and again just after delivering an Rh positive baby.

36. ***Concept Check 43.4***

1) Explain why a person who has type AB blood is considered a universal blood recipient.
Because individuals with type AB blood do not produce antibodies against either the A or the B antigens, they
can safely receive type A blood, type B blood, type AB blood, or type O blood-that is they are universal
recipients. In the case of donated type O blood, packed cells should be used, since the donor serum(fluid
part of the blood) would contain antibodies to A and to B, which could react with the recipients red blood
cells.
2) In bone marrow transplantation, there is a danger of a graft versus host reaction. Why is this reaction particular to a
bone marrow transplant
The danger of the graft rejecting the host arises because transplanted bone marrow contains lymphocytes
that could react against components of the recipients body.
3) Severely burned patients generally must receive numerous skin grafts. What is the advantage of using skin from an
unburned part of a patients own body rather then from another person.
An autograft will not trigger a rejection reaction.

37. Describe an allergic reaction, including the roles of IgE, mast cells, and histamine.
Allergies are exaggerated (hypersensitive) responses to certain antigens called allergens. The most common
allergies involve antibodies of the IgE class. These IgE cells can induce mast cells to release histamine and other
inflammatory agents. Histamine release causes dilation and increase permeability of small blood vessels and
lead to the typical symptoms sneezing, runny nose, tearing eyes and smooth muscle contractions.

38.
39. List three autoimmune disorders and describe possible mechanisms of autoimmunity.
In some individuals the immune system loses tolerance for self and turns against cetain molecules of the body
causing one of the many autoimmune diseases.
These include Lupus, arthritis and insulin dependent diabetes.

40.

41. Explain how general health and mental well-being might affect the immune system.
Healthy immune function appears to depend on both the endocrine system and the nervous system. Hormones
secreted by the adrenal glands during stress affect the numbers of white blood cells and may suppress the
immune system in other ways. Likewise in the nervous systems, some neurotransmitters secreted when we are
relaxed and happy may enhance immunity.

42. Describe the infectious agent that causes AIDS and explain how it enters a susceptible cell.
AIDS arises from the loss of helper T cells, both humoral and cell mediated immune responses are impaired. The
loss of helper T cells results from the infection by HIV. HIV gains entry into cells by making use of three proteins
that participate in normal immune responses. The main receptor for HIV on helper T cells is the cell’s CD4
molecule. The virus also infects other cell types such as macrophages and brain cells, that have low levels of
CD4. In addition to CD4, HIV entry requires a second cell surface protein, a co-receptor. One co-receptor called
fusin is present on all the cell types infected by HIV, while a different co receptor is present only on marcophages
and helper T cells.

43. Explain how HIV is transmitted and describe its incidence throughout the world. Note strategies that can reduce a person’s
risk of infection.
Transmission of HIV requires the transfer of body fluids containing infected cells, such as semen or blood from
person to person. Unprotected sex and sharing of needles are the most common forms. 40 million people
worldwide are living with HIV/AIDS. The best approach for slowing the spread of HIV is to educate people about
the practices that transmit the virus such as using a dirty needle or unprotected sex.

***Concept Check 43.5***

1) How would a macrophage deficiency likely affect a persons innate and acquired defenses
A person with a macrophage deficiency would have frequent infections. This would be due to poor innate
responses, particularly diminished phagocytosis and inflammation and poor acquired responses because of
the role of macrophages in presenting antigens to helper T cells.
2) Many anti allergy medications block response by mast cells. Explain why these drugs are effective in treating
allergies such as Hay Fever.
Binding of antigens by IgE molecules attached to mast cells induces degranulation of these cells, releasing
histamine and other inflammatory agents, which cause typical allergy symptoms. Drugs that block the
degranulation response prevent the release of inflammatory agents and hence the symptoms they cause.
3) In myasthenia gravis, antibodies bind to and block acetylcholine receptors at neuromuscular junctions, preventing
muscle contraction. Is this disease best classified as an immunodeficiency disease, an auto-immune disease or an
allergic disease? Explain
Myasthenia gravis is considered an autoimmune disease because the immune system produces antibodies
against self molecules
4) People who are nonfunction chemokine receptors because of genetic mutations are immune to HIV infection. Explain
this finding.
To enter a host cell, HIV requires CD4 and a co-receptor. The co-receptor for HIV normally functions as a
chemokine receptor. If a persons chemokine receptors are faulty, HIV cannot use them for entry into cells.